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  1. Extraction and application of keratin from natural resources: a review
    Chilakamarry CR, Mahmood S, Saffe SNBM, Arifin MAB, Gupta A, Sikkandar MY, et al.
    3 Biotech, 2021 May;11(5):220.
    PMID: 33968565 DOI: 10.1007/s13205-021-02734-7
    Over recent years, keratin has gained great popularity due to its exceptional biocompatible and biodegradable nature. It has shown promising results in various industries like poultry, textile, agriculture, cosmetics, and pharmaceutical. Keratin is a multipurpose biopolymer that has been used in the production of fibrous composites, and with necessary modifications, it can be developed into gels, films, nanoparticles, and microparticles. Its stability against enzymatic degradation and unique biocompatibility has found their way into biomedical applications and regenerative medicine. This review discusses the structure of keratin, its classification and its properties. It also covers various methods by which keratin is extracted like chemical hydrolysis, enzymatic and microbial treatment, dissolution in ionic liquids, microwave irradiation, steam explosion technique, and thermal hydrolysis or superheated process. Special emphasis is placed on its utilisation in the form of hydrogels, films, fibres, sponges, and scaffolds in various biotechnological and industrial sectors. The present review can be noteworthy for the researchers working on natural protein and related usage.
    Matched MeSH terms: Cytoskeleton
  2. A new species of the Simulium (Simulium) variegatum species-group (Diptera: Simuliidae) from Thailand
    Takaoka H, Srisuka W, Saeung A
    Acta Trop, 2019 Mar;191:155-161.
    PMID: 30611713 DOI: 10.1016/j.actatropica.2019.01.002
    A new species of black fly, Simulium (Simulium) luculentum, is described from specimens collected in Thailand, and is assigned to the Simulium variegatum species-group of the subgenus Simulium Latreille. This new species is distinguished from most members of this species group in the female by the mid femur and tibia entirely yellowish; and in the pupa by the gill with six filaments, which are somewhat inflated basally. This species represents the fifth member of the S. variegatum species-group recorded from Thailand.
    Matched MeSH terms: Cytoskeleton
  3. Fulltext Dentinogenic Ghost Cell Tumor in a Sumatran Rhinoceros
    Salleh A, Zainuddin ZZ, Tarmizi RMM, Yap CK, Jeng CR, Zamri-Saad M
    Animals (Basel), 2021 Apr 20;11(4).
    PMID: 33923894 DOI: 10.3390/ani11041173
    An adult female Sumatran rhinoceros was observed with a swelling in the left infraorbital region in March 2017. The swelling rapidly grew into a mass. A radiograph revealed a cystic radiolucent area in the left maxilla. In June 2017, the rhinoceros was euthanized. At necropsy, the infraorbital mass measured 21 cm × 30 cm. Samples of the infraorbital mass, left parotid gland, and left masseter muscle were collected for histopathology (Hematoxylin & Eosin, Von Kossa, Masson's trichrome, cytokeratin AE1/AE3, EMA, p53, and S-100). Numerous neoplastic epithelial cells showing pleomorphism and infiltration were observed. Islands of dentinoid material containing ghost cells and keratin pearls were observed with the aid of the two special histochemistry stains. Mitotic figures were rarely observed. All the neoplastic odontogenic cells and keratin pearls showed an intense positive stain for cytokeratin AE1/AE3, while some keratin pearls showed mild positive stains for S-100. All samples were negative for p53 and S-100 immunodetection. The mass was diagnosed as a dentinogenic ghost cell tumor.
    Matched MeSH terms: Cytoskeleton
  4. Investigation of the links between heterocyst and biohydrogen production by diazotrophic cyanobacterium A. variabilis ATCC 29413
    Salleh SF, Kamaruddin A, Uzir MH, Karim KA, Mohamed AR
    Arch Microbiol, 2016 Mar;198(2):101-13.
    PMID: 26521065 DOI: 10.1007/s00203-015-1164-6
    This work investigates the effect of heterocyst toward biohydrogen production by A. variabilis. The heterocyst frequency was artificially promoted by adding an amino acid analog, in this case DL-7-azatryptophan into the growth medium. The frequency of heterocyst differentiation was found to be proportional to the concentration of azatryptophan (0-25 µM) in the medium. Conversely, the growth and nitrogenase activity were gradually suppressed. In addition, there was also a distinct shortening of the cells filaments and detachment of heterocyst from the vegetative cells. Analysis on the hydrogen production performance revealed that both the frequency and distribution of heterocyst in the filaments affected the rate of hydrogen production. The highest hydrogen production rate and yield (41 µmol H2 mg chl a(-1) h(-1) and 97 mL H2 mg chl a(-1), respectively) were achieved by cells previously grown in 15 µM of azatryptophan with 14.5 % of heterocyst frequency. The existence of more isolated heterocyst has been shown to cause a relative loss in nitrogenase activity thus lowering the hydrogen production rate.
    Matched MeSH terms: Cytoskeleton
  5. Fulltext Edible bird's nest modulate intracellular molecular pathways of influenza A virus infected cells
    Haghani A, Mehrbod P, Safi N, Kadir FA, Omar AR, Ideris A
    BMC Complement Altern Med, 2017 Jan 05;17(1):22.
    PMID: 28056926 DOI: 10.1186/s12906-016-1498-x
    BACKGROUND: Edible Bird's Nest (EBN) as a popular traditional Chinese medicine is believed to have health enhancing and antiviral activities against influenza A virus (IAV); however, the molecular mechanism behind therapeutic effects of EBN is not well characterized.

    METHODS: In this study, EBNs that underwent different enzymatic preparation were tested against IAV infected cells. 50% cytotoxic concentration (CC50) and 50% inhibitory concentration (IC50) of the EBNs against IAV strain A/Puerto Rico/8/1934(H1N1) were determined by HA and MTT assays. Subsequently, the sialic acid content of the used EBNs were analyzed by fluorometric HPLC. Western Blotting and immunofluorescent staining were used to investigate the effects of EBNs on early endosomal trafficking and autophagy process of influenza virus.

    RESULTS: This study showed that post inoculations of EBNs after enzymatic preparations have the highest efficacy to inhibit IAV. While CC50 of the tested EBNs ranged from 27.5-32 mg/ml, the IC50 of these compounds ranged between 2.5-4.9 mg/ml. EBNs could inhibit IAV as efficient as commercial antiviral agents, such as amantadine and oseltamivir with different mechanisms of action against IAV. The antiviral activity of these EBNs correlated with the content of N-acetyl neuraminic acid. EBNs could affect early endosomal trafficking of the virus by reducing Rab5 and RhoA GTPase proteins and also reoriented actin cytoskeleton of IAV infected cells. In addition, for the first time this study showed that EBNs can inhibit intracellular autophagy process of IAV life cycle as evidenced by reduction of LC3-II and increasing of lysosomal degradation.

    CONCLUSIONS: The results procured in this study support the potential of EBNs as supplementary medication or alternative to antiviral agents to inhibit influenza infections. Evidently, EBNs can be a promising antiviral agent; however, these natural compounds should be screened for their metabolites prior to usage as therapeutic approach.

    Matched MeSH terms: Actin Cytoskeleton/drug effects; Actin Cytoskeleton/metabolism
  6. Fulltext The involvement of microtubules and actin during the infection of Japanese encephalitis virus in neuroblastoma cell line, IMR32
    Henry Sum MS
    Biomed Res Int, 2015;2015:695283.
    PMID: 25705678 DOI: 10.1155/2015/695283
    The role of the cytoskeleton, actin, and microtubules were examined during the process of Japanese encephalitis (JEV) infection in a human neuroblastoma cell line, IMR32. Cytochalasin D and nocodazole were used to depolymerise the cellular actin and microtubules, respectively, in order to study the effect of JEV infection in the cell. This study shows that depolymerisation of the actin cytoskeleton at early process of infection inhibits JEV infection in the cell; however infection was not inhibited when depolymerisation occurred at the later stage of infection. The microtubules, on the other hand, are required at 2 points in infection. The antigen production in the cells was inhibited when the infected cells were treated at time up to 2 hours after inoculation and there was no significant effect at later times, while the viable virus released continued to be affected until 10 hours after inoculation. In conclusion, infection of JEV in IMR32 cells required actin to facilitate early process in infection and the microtubular network is utilised as the transport system to the virus replication site and the release of mature virus.
    Matched MeSH terms: Actin Cytoskeleton/drug effects*
  7. Fulltext Interaction between Flavivirus and Cytoskeleton during Virus Replication
    Foo KY, Chee HY
    Biomed Res Int, 2015;2015:427814.
    PMID: 26347881 DOI: 10.1155/2015/427814
    Flaviviruses are potentially human pathogens that cause major epidemics worldwide. Flavivirus interacts with host cell factors to form a favourable virus replication site. Cell cytoskeletons have been observed to have close contact with flaviviruses, which expands the understanding of cytoskeleton functions during virus replication, although many detailed mechanisms are still unclear. The interactions between the virus and host cytoskeletons such as actin filaments, microtubules, and intermediate filaments have provided insight into molecular alterations during the virus infection, such as viral entry, in-cell transport, scaffold assembly, and egress. This review article focuses on the utilization of cytoskeleton by Flavivirus and the respective functions during virus replication.
    Matched MeSH terms: Cytoskeleton/metabolism*
  8. Fulltext Molecular subversion of Cdc42 signalling in cancer
    Murphy NP, Binti Ahmad Mokhtar AM, Mott HR, Owen D
    Biochem Soc Trans, 2021 06 30;49(3):1425-1442.
    PMID: 34196668 DOI: 10.1042/BST20200557
    Cdc42 is a member of the Rho family of small GTPases and a master regulator of the actin cytoskeleton, controlling cell motility, polarity and cell cycle progression. This small G protein and its regulators have been the subject of many years of fruitful investigation and the advent of functional genomics and proteomics has opened up new avenues of exploration including how it functions at specific locations in the cell. This has coincided with the introduction of new structural techniques with the ability to study small GTPases in the context of the membrane. The role of Cdc42 in cancer is well established but the molecular details of its action are still being uncovered. Here we review alterations found to Cdc42 itself and to key components of the signal transduction pathways it controls in cancer. Given the challenges encountered with targeting small G proteins directly therapeutically, it is arguably the regulators of Cdc42 and the effector signalling pathways downstream of the small G protein which will be the most tractable targets for therapeutic intervention. These will require interrogation in order to fully understand the global signalling contribution of Cdc42, unlock the potential for mapping new signalling axes and ultimately produce inhibitors of Cdc42 driven signalling.
    Matched MeSH terms: Actin Cytoskeleton/metabolism
  9. Fulltext Unearthing the role of septins in viral infections
    Khairat JE, Hatta MNA, Abdullah N, Azman AS, Calvin SYM, Syed Hassan S
    Biosci Rep, 2024 Mar 29;44(3).
    PMID: 38372298 DOI: 10.1042/BSR20231827
    Septin proteins are a subfamily of closely related GTP-binding proteins conserved in all species except for higher plants and perform essential biological processes. Septins self-assemble into heptameric or octameric complexes and form higher-order structures such as filaments, rings, or gauzes by end-to-end binding. Their close association with cell membrane components makes them central in regulating critical cellular processes. Due to their organisation and properties, septins function as diffusion barriers and are integral in providing scaffolding to support the membrane's curvature and stability of its components. Septins are also involved in vesicle transport and exocytosis through the plasma membrane by co-localising with exocyst protein complexes. Recently, there have been emerging reports of several human and animal diseases linked to septins and abnormalities in their functions. Most of our understanding of the significance of septins during microbial diseases mainly pertains to their roles in bacterial infections but not viruses. This present review focuses on the known roles of septins in host-viral interactions as detailed by various studies.
    Matched MeSH terms: Cytoskeleton/metabolism
  10. Mechano-cytoskeleton remodeling mechanism and molecular docking studies on nanosurface technology: Titania nanotube arrays
    Mydin RBSMN, Mahboob A, Sreekantan S, Saharudin KA, Qazem EQ, Hazan R, et al.
    Biotechnol Appl Biochem, 2023 Jun;70(3):1072-1084.
    PMID: 36567620 DOI: 10.1002/bab.2421
    In biomedical implant technology, nanosurface such as titania nanotube arrays (TNA) could provide better cellular adaptation, especially for long-term tissue acceptance response. Mechanotransduction activities of TNA nanosurface could involve the cytoskeleton remodeling mechanism. However, there is no clear insight into TNA mechano-cytoskeleton remodeling activities, especially computational approaches. Epithelial cells have played critical interface between biomedical implant surface and tissue acceptance, particularly for long-term interaction. Therefore, this study investigates genomic responses that are responsible for cell-TNA mechano-stimulus using epithelial cells model. Findings suggested that cell-TNA interaction may improve structural and extracellular matrix (ECM) support on the cells as an adaptive response toward the nanosurface topography. More specifically, the surface topography of the TNA might improve the cell polarity and adhesion properties via the interaction of the plasma membrane and intracellular matrix responses. TNA nanosurface might engross the cytoskeleton remodeling activities for multidirectional cell movement and cellular protrusions on TNA nanosurface. These observations are supported by the molecular docking profiles that determine proteins' in silico binding mechanism on TNA. This active cell-surface revamping would allow cells to adapt to develop a protective barrier toward TNA nanosurface, thus enhancing biocompatibility properties distinctly for long-term interaction. The findings from this study will be beneficial toward nano-molecular knowledge of designing functional nanosurface technology for advanced medical implant applications.
    Matched MeSH terms: Cytoskeleton
  11. In vitro anticancer properties and biological evaluation of novel natural alkaloid jerantinine B
    Qazzaz ME, Raja VJ, Lim KH, Kam TS, Lee JB, Gershkovich P, et al.
    Cancer Lett, 2016 Jan 28;370(2):185-97.
    PMID: 26515390 DOI: 10.1016/j.canlet.2015.10.013
    Natural products play a pivotal role in medicine especially in the cancer arena. Many drugs that are currently used in cancer chemotherapy originated from or were inspired by nature. Jerantinine B (JB) is one of seven novel Aspidosperma indole alkaloids isolated from the leaf extract of Tabernaemontana corymbosa. Preliminary antiproliferative assays revealed that JB and JB acetate significantly inhibited growth and colony formation, accompanied by time- and dose-dependent apoptosis induction in human cancer cell lines. JB significantly arrested cells at the G2/M cell cycle phase, potently inhibiting tubulin polymerisation. Polo-like kinase 1 (PLK1; an early trigger for the G2/M transition) was also dose-dependently inhibited by JB (IC50 1.5 µM). Furthermore, JB provoked significant increases in reactive oxygen species (ROS). Annexin V+ cell populations, dose-dependent accumulation of cleaved-PARP and caspase 3/7 activation, and reduced Bcl-2 and Mcl-1 expression confirm apoptosis induction. Preclinical in silico biopharmaceutical assessment of JB calculated rapid absorption and bioavailability >70%. Doses of 8-16 mg/kg JB were predicted to maintain unbound plasma concentrations >GI50 values in mice during efficacy studies. These findings advocate continued development of JB as a potential chemotherapeutic agent.
    Matched MeSH terms: Cytoskeleton/drug effects
  12. Improvement of early cell adhesion on Thai silk fibroin surface by low energy plasma
    Amornsudthiwat P, Mongkolnavin R, Kanokpanont S, Panpranot J, Wong CS, Damrongsakkul S
    Colloids Surf B Biointerfaces, 2013 Nov 1;111:579-86.
    PMID: 23893032 DOI: 10.1016/j.colsurfb.2013.07.009
    Low energy plasma has been introduced to treat the surface of Thai silk fibroin which should be enhanced for cell adhesion due to its native hydrophobic surface. Plasma surface treatment could introduce desirable hydrophilic functionalities on the surface without using any chemicals. In this work, nitrogen glow discharge plasma was generated by a low energy AC50Hz power supply system. The plasma operating conditions were optimized to reach the highest nitrogen active species by using optical emission spectroscopy. X-ray photoelectron spectroscopy (XPS) revealed that amine, hydroxyl, ether, and carboxyl groups were induced on Thai silk fibroin surface after plasma treatment. The results on Fourier transform infrared attenuated total reflection (FTIR-ATR) spectroscopy confirmed that the plasma treated effects were only on the outermost layer since there was no change in the bulk chemistry. The surface topography was insignificantly changed from the detection with atomic force microscopy (AFM). The plasma-treated effects were the improved surface wettability and cell adhesion. After a 90-s treatment, the water contact angle was at 20°, while the untreated surface was at 70°. The early cell adhesion of L929 mouse fibroblast was accelerated. L929 cells only took 3h to reach 100% cell adhesion on 90 s N2 plasma-treated surface, while there was less than 50% cell adhesion on the untreated Thai silk fibroin surface after 6h of culture. The cell adhesion results were in agreement with the cytoskeleton development. L929 F-actin was more evident on 90 s N2 plasma-treated surface than others. It could be concluded that a lower energy AC50Hz plasma system enhanced early L929 mouse fibroblast adhesion on Thai silk fibroin surface without any significant change in surface topography and bulk chemistry.
    Matched MeSH terms: Cytoskeleton/drug effects; Cytoskeleton/metabolism
  13. The role of host microfilaments and microtubules during opsonin-independent interactions of Cryptococcus neoformans with mammalian lung cells
    Choo KK, Chong PP, Ho AS, Yong PV
    Eur J Clin Microbiol Infect Dis, 2015 Dec;34(12):2421-7.
    PMID: 26463450 DOI: 10.1007/s10096-015-2497-4
    The purpose of this investigation was to characterise the interactions of Cryptococcus neoformans with mammalian host alveolar epithelial cells and alveolar macrophages, with emphasis on the roles of the cryptococcal capsule and the host cell cytoskeletons. The adherence and internalisation of C. neoformans into mammalian lung cells and the roles of host cell cytoskeletons in host-pathogen interactions were studied using in vitro models coupled with a differential fluorescence assay, fluorescence staining, immunofluorescence and drug inhibition of actin and microtubule polymerisation. Under conditions devoid of opsonin and macrophage activation, C. neoformans has a high affinity towards MH-S alveolar macrophages, yet associated poorly to A549 alveolar epithelial cells. Acapsular C. neoformans adhered to and internalised into the mammalian cells more effectively compared to encapsulated cryptococci. Acapsular C. neoformans induced prominent actin reorganisation at the host-pathogen interface in MH-S alveolar macrophages, but minimally affected actin reorganisation in A549 alveolar epithelial cells. Acapsular C. neoformans also induced localisation of microtubules to internalised cryptococci in MH-S cells. Drug inhibition of actin and microtubule polymerisation both reduced the association of acapsular C. neoformans to alveolar macrophages. The current study visualises and confirms the interactions of C. neoformans with mammalian alveolar cells during the establishment of infection in the lungs. The acapsular form of C. neoformans effectively adhered to and internalised into alveolar macrophages by inducing localised actin reorganisation, relying on the host's actin and microtubule activities.
    Matched MeSH terms: Cytoskeleton
  14. Momordica charantia (Indian and Chinese Bitter Melon) Extracts Inducing Apoptosis in Human Lung Cancer Cell Line A549 via ROS-Mediated Mitochodria Injury
    Thiagarajan S, Arapoc DJ, Husna Shafie N, Keong YY, Bahari H, Adam Z, et al.
    Evid Based Complement Alternat Med, 2019;2019:2821597.
    PMID: 30956678 DOI: 10.1155/2019/2821597
    Lung cancer is the leading cause of cancer related deaths worldwide with about 40% occurring in developing countries. The two varieties of Momordica charantia, which are Chinese and Indian bitter melon, have been subjected to antiproliferative activity in human non-small cell lung cells A549. The A549 cells were treated with hot and cold aqueous extraction for both the bitter melon varieties, and the antiproliferative activity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptotic mechanism of action on A549 human lung cancer cells was evaluated first morphologically using Hoechst 33358, and cytoskeleton staining using Filamentous-actin (F-actin) cytoskeleton FICT and DAPI followed by caspase-3/7, reactive oxygen species (ROS), and p53 activity. Chinese hot aqueous extraction (CHA) exhibited potent antiproliferative activity against A549 human lung cancer cells. The morphological analysis of mitochondria destruction and the derangement of cytoskeleton showed apoptosis-inducing activity. CHA increased the caspase-3/7 activity by 1.6-fold and the ROS activity by 5-fold. Flow cytometric analysis revealed 34.5% of apoptotic cells significantly (p<0.05) compared to cisplatin-treated A549 human cancer cells. CHA is suggested to induce apoptosis due to their rich bioactive chemical constituents. These findings suggest that the antiproliferative effect of CHA was due to apoptosis via ROS-mediated mitochondria injury.
    Matched MeSH terms: Cytoskeleton
  15. Orbital fluid shear stress promotes osteoblast metabolism, proliferation and alkaline phosphates activity in vitro
    Aisha MD, Nor-Ashikin MN, Sharaniza AB, Nawawi H, Froemming GR
    Exp Cell Res, 2015 Sep 10;337(1):87-93.
    PMID: 26163894 DOI: 10.1016/j.yexcr.2015.07.002
    Prolonged disuse of the musculoskeletal system is associated with reduced mechanical loading and lack of anabolic stimulus. As a form of mechanical signal, the multidirectional orbital fluid shear stress transmits anabolic signal to bone forming cells in promoting cell differentiation, metabolism and proliferation. Signals are channeled through the cytoskeleton framework, directly modifying gene and protein expression. For that reason, we aimed to study the organization of Normal Human Osteoblast (NHOst) cytoskeleton with regards to orbital fluid shear (OFS) stress. Of special interest were the consequences of cytoskeletal reorganization on NHOst metabolism, proliferation, and osteogenic functional markers. Cells stimulated at 250 RPM in a shaking incubator resulted in the rearrangement of actin and tubulin fibers after 72 h. Orbital shear stress increased NHOst mitochondrial metabolism and proliferation, simultaneously preventing apoptosis. The ratio of RANKL/OPG was reduced, suggesting that orbital shear stress has the potential to inhibit osteoclastogenesis and osteoclast activity. Increase in ALP activity and OCN protein production suggests that stimulation retained osteoblast function. Shear stress possibly generated through actin seemed to hold an anabolic response as osteoblast metabolism and functional markers were enhanced. We hypothesize that by applying orbital shear stress with suitable magnitude and duration as a non-drug anabolic treatment can help improve bone regeneration in prolonged disuse cases.
    Matched MeSH terms: Cytoskeleton/metabolism; Cytoskeleton/ultrastructure
  16. Short-term moderate hypothermia stimulates alkaline phosphatase activity and osteocalcin expression in osteoblasts by upregulating Runx2 and osterix in vitro
    Aisha MD, Nor-Ashikin MN, Sharaniza AB, Nawawi HM, Kapitonova MY, Froemming GR
    Exp Cell Res, 2014 Aug 1;326(1):46-56.
    PMID: 24928274 DOI: 10.1016/j.yexcr.2014.06.003
    Exposure of Normal Human Osteoblast cells (NHOst) to a period of hypothermia may interrupt their cellular functions, lead to changes in bone matrix and disrupt the balance between bone formation and resorption, resulting in bone loss or delayed fracture healing. To investigate this possibility, we exposed NHOst cells to moderate (35 °C) and severe (27 °C) hypothermia for 1, 12, 24 and 72 h. The effects of hypothermia with respect to cell cytoskeleton organization, metabolic activity and the expression of cold shock chaperone proteins, osteoblast transcription factors and functional markers, were examined. Our findings showed that prolonged moderate hypothermia retained the polymerization of the cytoskeletal components. NHOst cell metabolism was affected differently according to hypothermia severity. The osteoblast transcription factors Runx2 and osterix were necessary for the transcription and translation of bone matrix proteins, where alkaline phosphatase (Alp) activity and osteocalcin (OCN) bone protein were over expressed under hypothermic conditions. Consequently, bone mineralization was stimulated after exposure to moderate hypothermia for 1 week, indicating bone function was not impaired. The cold shock chaperone protein Rbm3 was significantly upregulated (p<0.001) during the cellular stress adaption under hypothermic conditions. We suggest that Rbm3 has a dual function: one as a chaperone protein that stabilizes mRNA transcripts and a second one in enhancing the transcription of Alp and Ocn genes. Our studies demonstrated that hypothermia permitted the in vitro maturation of NHOst cells probably through an osterix-dependent pathway. For that reason, we suggest that moderate hypothermia can be clinically applied to counteract heat production at the fracture site that delays fracture healing.
    Matched MeSH terms: Cytoskeleton/metabolism
  17. Fulltext Differential Regulation of LPS-Mediated VE-Cadherin Disruption in Human Endothelial Cells and the Underlying Signaling Pathways: A Mini Review
    Chan YH, Harith HH, Israf DA, Tham CL
    Front Cell Dev Biol, 2019;7:280.
    PMID: 31970155 DOI: 10.3389/fcell.2019.00280
    Endothelial cells lining the inner vascular wall form a monolayer that contributes to the selective permeability of endothelial barrier. This selective permeability is mainly regulated by an endothelium-specific adherens junctional protein, known as vascular endothelial-cadherin (VE-cadherin). In endothelial cells, the adherens junction comprises of VE-cadherin and its associated adhesion molecules such as p120, α-catenin, and β-catenin, in which α-catenin links cytoplasmic tails of VE-cadherin to actin cytoskeleton through β-catenin. Proinflammatory stimuli such as lipopolysaccharide (LPS) are capable of attenuating vascular integrity through the disruption of VE-cadherin adhesion in endothelial cells. To date, numerous studies demonstrated the disruption of adherens junction as a result of phosphorylation-mediated VE-cadherin disruption. However, the outcomes from these studies were inconsistent and non-conclusive as different cell fractions were used to examine the effect of LPS on the disruption of VE-cadherin. By using Western Blot, some studies utilized total protein lysate and reported decreased protein expression while some studies reported unchanged expression. Other studies which used membrane and cytosolic fractions of protein extract demonstrated decreased and increased VE-cadherin expression, respectively. Despite the irregularities, the results of immunofluorescence staining are consistent with the formation of intercellular gap. Besides that, the overall underlying disruptive mechanisms of VE-cadherin remain largely unknown. Therefore, this mini review will focus on different experiment approaches in terms of cell fractions used in different human endothelial cell studies, and relate these differences to the results obtained in Western blot and immunofluorescence staining in order to give some insights into the overall differential regulatory mechanisms of LPS-mediated VE-cadherin disruption and address the discrepancy in VE-cadherin expression.
    Matched MeSH terms: Actin Cytoskeleton
  18. Fulltext Simvastatin modulates cellular components in influenza A virus-infected cells
    Mehrbod P, Hair-Bejo M, Tengku Ibrahim TA, Omar AR, El Zowalaty M, Ajdari Z, et al.
    Int J Mol Med, 2014 Jul;34(1):61-73.
    PMID: 24788303 DOI: 10.3892/ijmm.2014.1761
    Influenza A virus is one of the most important health risks that lead to significant respiratory infections. Continuous antigenic changes and lack of promising vaccines are the reasons for the unsuccessful treatment of influenza. Statins are pleiotropic drugs that have recently served as anti-influenza agents due to their anti-inflammatory activity. In this study, the effect of simvastatin on influenza A-infected cells was investigated. Based on the MTT cytotoxicity test, hemagglutination (HA) assay and qPCR it was found that simvastatin maintained cell viability and decreased the viral load significantly as compared to virus-inoculated cells. The expression of important pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6 and interferon-γ), which was quantified using ELISA showed that simvastatin decreased the expression of pro-inflammatory cytokines to an average of 2-fold. Furthermore, the modulation of actin filament polymerization was determined using rhodamine staining. Endocytosis and autophagy processes were examined by detecting Rab and RhoA GTPase protein prenylation and LC3 lipidation using western blotting. The results showed that inhibiting GTPase and LC3 membrane localization using simvastatin inhibits influenza replication. Findings of this study provide evidence that modulation of RhoA, Rabs and LC3 may be the underlying mechanisms for the inhibitory effects of simvastatin as an anti-influenza compound.
    Matched MeSH terms: Actin Cytoskeleton/genetics; Actin Cytoskeleton/metabolism
  19. Barrier protective effects of 2,4,6-trihydroxy-3-geranyl acetophenone on lipopolysaccharides-stimulated inflammatory responses in human umbilical vein endothelial cells
    Chong YJ, Musa NF, Ng CH, Shaari K, Israf DA, Tham CL
    J Ethnopharmacol, 2016 Nov 04;192:248-255.
    PMID: 27404229 DOI: 10.1016/j.jep.2016.07.032
    PHARMOCOLOGICAL RELEVANCE: 2,4,6-trihydroxy-3-geranyl acetophenone (tHGA), is a phloroglucinol compound found naturally in Melicope ptelefolia. Melicope ptelefolia has been used traditionally for centuries as natural remedy for wound infections and inflammatory diseases.

    AIM OF THE STUDY: Endothelial barrier dysfunction is a pathological hallmark of many diseases and can be caused by lipopolysaccharides (LPS) stimulation. Therefore, this study aims to investigate the possible barrier protective effects of tHGA upon LPS-stimulated inflammatory responses in human umbilical vein endothelial cells (HUVECs).

    MATERIALS AND METHODS: HUVECs were pretreated with tHGA prior to LPS stimulation, where inflammatory parameters including permeability, monocyte adhesion and migration, and release of pro-inflammatory mediators were examined. Additionally, the effect of tHGA on F-actin rearrangement and adhesion protein expression of LPS-stimulated HUVECs was evaluated.

    RESULTS: It was found that pretreatment with tHGA inhibited monocyte adhesion and transendothelial migration, reduced endothelial hyperpermeability and secretion of prostaglandin E2 (PGE2). Additionally, tHGA inhibited cytoskeletal rearrangement and adhesion protein expression on LPS-stimulated HUVECs.

    CONCLUSION: As the regulation of endothelial barrier dysfunction can be one of the therapeutic strategies to improve the outcome of inflammation, tHGA may be able to preserve vascular barrier integrity of endothelial cells following LPS-stimulated dysfunction, thereby endorsing its potential usefulness in vascular inflammatory diseases.

    Matched MeSH terms: Actin Cytoskeleton/drug effects; Actin Cytoskeleton/metabolism
  20. Interferon-Gamma Increases Endothelial Permeability by Causing Activation of p38 MAP Kinase and Actin Cytoskeleton Alteration
    Ng CT, Fong LY, Sulaiman MR, Moklas MA, Yong YK, Hakim MN, et al.
    J Interferon Cytokine Res, 2015 Jul;35(7):513-22.
    PMID: 25830506 DOI: 10.1089/jir.2014.0188
    Interferon-gamma (IFN-γ) is known to potentiate the progression of inflammatory diseases, such as inflammatory bowel disease and atherosclerosis. IFN-γ has been found to disrupt the barrier integrity of epithelial and endothelial cell both in vivo and in vitro. However, the mechanisms of IFN-γ underlying increased endothelial cell permeability have not been extensively elucidated. We reported that IFN-γ exhibits a biphasic nature in increasing endothelial permeability. The changes observed in the first phase (4-8 h) involve cell retraction and rounding in addition to condensed peripheral F-actin without a significant change in the F-/G-actin ratio. However, cell elongation, stress fiber formation, and an increased F-/G-actin ratio were noticed in the second phase (16-24 h). Consistent with our finding from the permeability assay, IFN-γ induced the formation of intercellular gaps in both phases. A delayed phase of increased permeability was observed at 12 h, which paralleled the onset of cell elongation, stress fiber formation, and increased F-/G-actin ratio. In addition, IFN-γ stimulated p38 mitogen-activated protein (MAP) kinase phosphorylation over a 24 h period. Inhibition of p38 MAP kinase by SB203580 prevented increases in paracellular permeability, actin rearrangement, and increases in the F-/G-actin ratio caused by IFN-γ. Our results suggest that p38 MAP kinase is activated in response to IFN-γ and causes actin rearrangement and altered cell morphology, which in turn mediates endothelial cell hyperpermeability. The F-/G-actin ratio might be involved in the regulation of actin distribution and cell morphology rather than the increased permeability induced by IFN-γ.
    Matched MeSH terms: Actin Cytoskeleton/drug effects; Actin Cytoskeleton/metabolism*
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