Displaying publications 1 - 20 of 80 in total

  1. Abd Rahman F, Mohd Ali J, Abdullah M, Abu Kasim NH, Musa S
    J. Periodontol., 2016 07;87(7):837-47.
    PMID: 26846966 DOI: 10.1902/jop.2016.150610
    BACKGROUND: This study investigates the effects of aspirin (ASA) on the proliferative capacity, osteogenic potential, and expression of growth factor-associated genes in periodontal ligament stem cells (PDLSCs).

    METHODS: Mesenchymal stem cells (MSCs) from PDL tissue were isolated from human premolars (n = 3). The MSCs' identity was confirmed by immunophenotyping and trilineage differentiation assays. Cell proliferation activity was assessed through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Polymerase chain reaction array was used to profile the expression of 84 growth factor-associated genes. Pathway analysis was used to identify the biologic functions and canonic pathways activated by ASA treatment. The osteogenic potential was evaluated through mineralization assay.

    RESULTS: ASA at 1,000 μM enhances osteogenic potential of PDLSCs. Using a fold change (FC) of 2.0 as a threshold value, the gene expression analyses indicated that 19 genes were differentially expressed, which includes 12 upregulated and seven downregulated genes. Fibroblast growth factor 9 (FGF9), vascular endothelial growth factor A (VEGFA), interleukin-2, bone morphogenetic protein-10, VEGFC, and 2 (FGF2) were markedly upregulated (FC range, 6 to 15), whereas pleotropin, FGF5, brain-derived neurotrophic factor, and Dickkopf WNT signaling pathway inhibitor 1 were markedly downregulated (FC 32). Of the 84 growth factor-associated genes screened, 35 showed high cycle threshold values (≥35).

    CONCLUSIONS: ASA modulates the expression of growth factor-associated genes and enhances osteogenic potential in PDLSCs. ASA upregulated the expression of genes that could activate biologic functions and canonic pathways related to cell proliferation, human embryonic stem cell pluripotency, tissue regeneration, and differentiation. These findings suggest that ASA enhances PDLSC function and may be useful in regenerative dentistry applications, particularly in the areas of periodontal health and regeneration.

    Matched MeSH terms: Vascular Endothelial Growth Factor A/physiology*
  2. Bastion ML, Then KY, Faridah HA, Mushawiahti M, Othmaliza O, Wong HS
    Med. J. Malaysia, 2011 Mar;66(1):10-4.
    PMID: 23765135 MyJurnal
    This retrospective study investigated the role of antivascular endothelial growth factor agents (VEGF), ranibizumab, bevacizumab and pegaptanib sodium in patients with iris neovascularisation (INV), in which 9 eyes received intraocular injections for various ischaemic ocular conditions. Ocular sequelae included recurrence of rubeosis (n=2) and hyphaema (n=2). Systemic complication included one case of cerebrovascular accident. INV regressed in all cases from day one. INV recurrence occurred in 2 cases. The mean intraocular pressure of the study eyes decreased from 25.3 mmHg to 18.3 mmHg at one month. Five eyes are medication free. Visual acuity improved in 5 eyes. Four eyes achieved a Snellen visual acuity of 6/24 or better. We conclude that the use of intraocular anti-VEGF agents are safe and effective for inducing the regression of INV. Patients with multiple systemic risk factors should be counseled on stroke risk.
    Matched MeSH terms: Vascular Endothelial Growth Factor A*
  3. Langmia IM, Apalasamy YD, Omar SZ, Mohamed Z
    Pharmacogenet. Genomics, 2015 Apr;25(4):199-204.
    PMID: 25714003 DOI: 10.1097/FPC.0000000000000125
    Angiogenic pathway regulating genes such as vascular endothelial growth factor A (VEGFA) have been implicated in preterm birth (PTB) complications. Research shows that the VEGFA/VEGF receptor system plays an important role in the regulation of circulating progesterone level. Attenuation of VEGFA signaling at mid pregnancy results in onset of labor and parturition because of a reduction in circulating progesterone levels. The aim of this study was to investigate the association of VEGFA gene polymorphisms (rs2010963, rs3025039, rs699947, and rs10434) with spontaneous PTB and VEGFA plasma levels in preterm and term women.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/blood*; Vascular Endothelial Growth Factor A/genetics*
  4. Ng CT, Yip WK, Mohtarrudin N, Seow HF
    Malays J Pathol, 2015 Dec;37(3):219-25.
    PMID: 26712666 MyJurnal
    Immortalized human endothelial cells are widely used as in vitro models for debilitating conditions such as cancer, cardiovascular and ocular diseases. Human microvascular endothelial cell (HMEC-1) is immortalized via stable transfection with a gene encoding SV40 large antigen whilst telomerase-immortalized human microvascular endothelial (TIME) cells is immortalized by engineering the human telomerase catalytic protein (hTERT) into primary microvascular endothelial cells. Here, we established a three-dimensional (3D) spheroid invasion assay with HMEC-1 and TIME and compared the difference in their ability to invade through the collagen matrix in response to exogenous growth factors, namely vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).
    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism*; Vascular Endothelial Growth Factor A/pharmacology
  5. Noranizah W, Siti-Aishah MA, Munirah MA, Norazlin MH, Rohaizak M, Naqiyah I, et al.
    Clin Ter, 2010;161(2):129-37.
    PMID: 20499026
    Vascular endothelial growth factor (VEGF) is a leading factor for tumour angiogenesis and p53 protein is the product of a tumor suppressor gene. The main aim of the study was to assess the association of p53 protein with VEGF expression in breast carcinoma.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/analysis*; Vascular Endothelial Growth Factor A/biosynthesis*
  6. Mohamad NA, Ramachandran V, Ismail P, Mohd Isa H, Chan YM, Ngah NF, et al.
    Genet Test Mol Biomarkers, 2017 Oct;21(10):600-607.
    PMID: 28926292 DOI: 10.1089/gtmb.2017.0079
    AIM: To determine the association of vascular endothelial growth factor (VEGF) polymorphisms with neovascular age-related macular degeneration (nAMD).

    MATERIALS AND METHODS: One hundred thirty-five nAMD patients and 135 controls were recruited to determine the association of the -460 C/T, the -2549 I/D, and the +405 G/C polymorphisms with the VEGF gene. Genotyping was conducted using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) approach, and association analyses were conducted using chi-square analysis and logistic regression analysis.

    RESULTS: A significant association was observed between nAMD and the VEGF +405 G/C genotypes (p = 0.002) and alleles (odds ratio = 1.36, 95% confidence interval = 1.12-1.62, p = < 0.001) compared with the controls. This association was confirmed by logistic regression analyses, using two different genetic models (additive and dominant) resulting in p-values of p = 0.001 and p 

    Matched MeSH terms: Vascular Endothelial Growth Factor A/genetics*; Vascular Endothelial Growth Factor A/metabolism
  7. Wong JG, Lai XJ, Sarafian RY, Wong HS, Smith JB
    Int Med Case Rep J, 2017;10:51-54.
    PMID: 28243154 DOI: 10.2147/IMCRJ.S107648
    We report a case of a Caucasian female who developed active polypoidal choroidal vasculopathy (PCV) at the edge of a stable choroidal nevus and was successfully treated with verteporfin photodynamic therapy. No active polyp was detectable on indocyanine green angiography 2 years after treatment, and good vision was maintained. Indocyanine green angiography is a useful investigation to diagnose PCV and may be underutilized. Unlike treatment of choroidal neovascularization secondary to choroidal nevus, management of PCV secondary to nevus may not require intravitreal anti-vascular endothelial growth factor therapy. Photodynamic monotherapy may be an effective treatment of secondary PCV.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  8. Azliana AF, Zainul-Rashid MR, Chandramaya SF, Farouk WI, Nurwardah A, Wong YP, et al.
    Indian J Pathol Microbiol, 2018 1 13;60(4):515-520.
    PMID: 29323064 DOI: 10.4103/IJPM.IJPM_376_16
    INTRODUCTION: Hypertensive disorder in pregnancy (HDP) represents the most common medical complication in pregnancy. It is the leading cause of maternal and perinatal mortality and morbidity. Vascular endothelial growth factor (VEGF) stimulates vascular endothelial cell growth, survival, and proliferation, and they are known to be expressed in human placenta. The aim of this study was to determine the VEGF expression in the placenta of hypertensive and normotensive patients.

    MATERIALS AND METHODS: This is a retrospective, cross-sectional study from January 1, 2015 to December 31, 2015. A total of 30 placentae comprised of 15 hypertensive and 15 normotensive cases were assessed. VEGF expression in placenta was assessed by immunohistochemistry, and the number of syncytial knots was counted.

    RESULTS: Our study showed an increased syncytial knot formation in the placenta of hypertensive mothers. VEGF expression was seen in syncytiotrophoblasts of 14 of the hypertensive cases (14/15, 93.3%), while only two of the normotensive cases were positive (2/15, 13.3%). There were no statistically significant differences in VEGF expression in other placenta cells, that is, cytotrophoblasts (P = 1.0), decidual cells (0.1394), maternal endothelial cells (0.5977), and fetal endothelial cells (P = 1.0).

    CONCLUSIONS: This study showed an increased number of syncytial knots is a consistent histological finding in the placenta of patient with HDP. VEGF expression was significantly increased in syncytiotrophoblasts in placenta of hypertensive group, and it could be used as a biomarker for hypertension.

    Matched MeSH terms: Vascular Endothelial Growth Factor A/analysis*
  9. Choi JR, Pingguan-Murphy B, Wan Abas WA, Yong KW, Poon CT, Noor Azmi MA, et al.
    PLoS ONE, 2015;10(1):e0115034.
    PMID: 25615717 DOI: 10.1371/journal.pone.0115034
    Adipose tissue-derived stromal cells (ASCs) natively reside in a relatively low-oxygen tension (i.e., hypoxic) microenvironment in human body. Low oxygen tension (i.e., in situ normoxia), has been known to enhance the growth and survival rate of ASCs, which, however, may lead to the risk of tumourigenesis. Here, we investigated the tumourigenic potential of ASCs under their physiological condition to ensure their safe use in regenerative therapy. Human ASCs isolated from subcutaneous fat were cultured in atmospheric O2 concentration (21% O2) or in situ normoxia (2% O2). We found that ASCs retained their surface markers, tri-lineage differentiation potential, and self-renewal properties under in situ normoxia without altering their morphology. In situ normoxia displayed a higher proliferation and viability of ASCs with less DNA damage as compared to atmospheric O2 concentration. Moreover, low oxygen tension significantly up-regulated VEGF and bFGF mRNA expression and protein secretion while reducing the expression level of tumour suppressor genes p16, p21, p53, and pRb. However, there were no significant differences in ASCs telomere length and their relative telomerase activity when cultured at different oxygen concentrations. Collectively, even with high proliferation and survival rate, ASCs have a low tendency of developing tumour under in situ normoxia. These results suggest 2% O2 as an ideal culture condition for expanding ASCs efficiently while maintaining their characteristics.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/genetics; Vascular Endothelial Growth Factor A/metabolism
  10. Wu LE, Meoli CC, Mangiafico SP, Fazakerley DJ, Cogger VC, Mohamad M, et al.
    Diabetes, 2014 Aug;63(8):2656-67.
    PMID: 24696450 DOI: 10.2337/db13-1665
    The vascular endothelial growth factor (VEGF) family of cytokines are important regulators of angiogenesis that have emerged as important targets for the treatment of obesity. While serum VEGF levels rise during obesity, recent studies using genetic models provide conflicting evidence as to whether VEGF prevents or accelerates metabolic dysfunction during obesity. In the current study, we sought to identify the effects of VEGF-A neutralization on parameters of glucose metabolism and insulin action in a dietary mouse model of obesity. Within only 72 h of administration of the VEGF-A-neutralizing monoclonal antibody B.20-4.1, we observed almost complete reversal of high-fat diet-induced insulin resistance principally due to improved insulin sensitivity in the liver and in adipose tissue. These effects were independent of changes in whole-body adiposity or insulin signaling. These findings show an important and unexpected role for VEGF in liver insulin resistance, opening up a potentially novel therapeutic avenue for obesity-related metabolic disease.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/genetics; Vascular Endothelial Growth Factor A/metabolism*
  11. Kamarulzaman EE, Vanderesse R, Gazzali AM, Barberi-Heyob M, Boura C, Frochot C, et al.
    J. Biomol. Struct. Dyn., 2017 Jan;35(1):26-45.
    PMID: 26766582 DOI: 10.1080/07391102.2015.1131196
    Vascular endothelial growth factor (VEGF) and its co-receptor neuropilin-1 (NRP-1) are important targets of many pro-angiogenic factors. In this study, nine peptides were synthesized and evaluated for their molecular interaction with NRP-1 and compared to our previous peptide ATWLPPR. Docking study showed that the investigated peptides shared the same binding region as shown by tuftsin known to bind selectively to NRP-1. Four pentapeptides (DKPPR, DKPRR, TKPPR and TKPRR) and a hexapeptide CDKPRR demonstrated good inhibitory activity against NRP-1. In contrast, peptides having arginine residue at sites other than the C-terminus exhibited low activity towards NRP-1 and this is confirmed by their inability to displace the VEGF165 binding to NRP-1. Docking study also revealed that replacement of carboxyl to amide group at the C-terminal arginine of the peptide did not affect significantly the binding interaction to NRP-1. However, the molecular affinity study showed that these peptides have marked reduction in the activity against NRP-1. Pentapeptides having C-terminal arginine showed strong interaction and good inhibitory activity with NRP thus may be a good template for anti-angiogenic targeting agent.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/antagonists & inhibitors; Vascular Endothelial Growth Factor A/chemistry
  12. Weng-Yew W, Selvaduray KR, Ming CH, Nesaretnam K
    Nutr Cancer, 2009;61(3):367-73.
    PMID: 19373610 DOI: 10.1080/01635580802582736
    Previous studies have revealed that tocotrienol-rich fractions (TRF) from palm oil inhibit the proliferation and the growth of solid tumors. The anticancer activity of TRF is said to be caused by several mechanisms, one of which is antiangiogenesis. In this study, we looked at the antiangiogenic effects of TRF. In vitro investigations of the antiangiogenic activities of TRF, delta-tocotrienol (deltaT3), and alpha-tocopherol (alphaToc) were carried out in human umbilical vein endothelial cells (HUVEC). TRF and deltaT3 significantly inhibited cell proliferation from 4 microg/ml onward (P < 0.05). Cell migration was inhibited the most by deltaT3 at 12 microg/ml. Anti-angiogenic properties of TRF were carried out further in vivo using the chick embryo chorioallantoic membrane (CAM) assay and BALB/c mice model. TRF at 200 microg/ml reduced the vascular network on CAM. TRF treatment of 1 mg/mouse significantly reduced 4T1 tumor volume in BALB/c mice. TRF significantly reduced serum vascular endothelial growth factor (VEGF) level in BALB/c mice. In conclusion, this study showed that palm tocotrienols exhibit anti-angiogenic properties that may assist in tumor regression.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/antagonists & inhibitors; Vascular Endothelial Growth Factor A/blood
  13. Nur Fariha MM, Chua KH, Tan GC, Lim YH, Hayati AR
    Cell Biol. Int., 2012;36(12):1145-53.
    PMID: 22957758 DOI: 10.1042/CBI20120044
    Cell-based therapy using stem cells has emerged as one of the pro-angiogenic methods to enhance blood vessel growth and sprouting in ischaemic conditions. This study investigated the endogenous and induced angiogenic characteristics of hCDSC (human chorion-derived stem cell) using QPCR (quantitative PCR) method, immunocytochemistry and fibrin-matrigel migration assay. The results showed that cultured hCDSC endogenously expressed angiogenic-endogenic-associated genes (VEGF, bFGF, PGF, HGF, Ang-1, PECAM-1, eNOS, Ve-cad, CD34, VEGFR-2 and vWF), with significant increase in mRNA levels of PGF, HGF, Ang-1, eNOS, VEGFR-2 and vWF following induction by bFGF (basic fibroblast growth factor) and VEGF (vascular endothelial growth factor). These enhanced angiogenic properties suggest that induced hCDSC provides a stronger angiogenic effect for the treatment of ischaemia. After angiogenic induction, hCDSC showed no reduction in the expression of the stemness genes, but had significantly higher levels of mRNA of Oct-4, Nanog (3), FZD9, ABCG-2 and BST-1. The induced cells were positive for PECAM-1 (platelet/endothelial cell adhesion molecule 1) and vWF (von Willebrand factor) with immunocytochemistry staining. hCDSC also showed endothelial migration behaviour when cultured in fibrin-matrigel construct and were capable of forming vessels in vivo after implanting into nude mice. These data suggest that hCDSC could be the cells of choice in the cell-based therapy for pro-angiogenic purpose.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/analysis; Vascular Endothelial Growth Factor A/genetics; Vascular Endothelial Growth Factor A/pharmacology*
  14. Md Hashim, S.N., Yusof, M.F.H., Alshehadat, S.A., Kannan, T.P., Azlina, A., Suzina, S.A.H., et al.
    Angiogenicity is one of the essential components to enable tissue function. It is important to develop a construct that would help in catering oxygen and nutrient to the engineered tissue area. Thus, this study aims to investigate the attachment, spreading and growth of stem cells from human exfoliated deciduous teeth (SHED) on human AM (HAM) with or without vascular endothelial growth factor (VEGF) using scanning electron microscope (SEM), and indirectly see the potential of the HAM as a scaffold to promote angiogenic micro-environment. Since day 1, there were continuous changes of the cell morphology until day 28, SHED treated with VEGF seemed to change its shape from fibroblast-like into a round-shape cell, similar structure as an endotheliallike cell. The structures of filopodia-like were also observed on the treated SHED. SHED without VEGF treatment showed only normal morphological growth on HAM. VEGF is a protein produced to stimulate angiogenesis, and is believed to contribute to the morphological changes of SHED seeded on HAM. This indicates that HAM could be used as a scaffold to allow SHED differentiation into endothelial-like cells with the induction of VEGF.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  15. Liau LL, Makpol S, Azurah AGN, Chua KH
    Cytotechnology, 2018 Aug;70(4):1221-1233.
    PMID: 29549558 DOI: 10.1007/s10616-018-0214-8
    Currently, orthotopic liver transplantation is the gold standard therapy for liver failure. However, it is limited by the insufficient organ donor and risk of immune rejection. Stem cell therapy is a promising alternative treatment for liver failure. One of the most ideal sources of stem cells for regenerative medicine is adipose-derived stem cells (ADSCs). In this study, primary ADSCs seeded on cell culture insert were indirectly co-cultured with injured HepG2 to elucidate the role of ADSCs in promoting the recovery of injured HepG2 in non-contact manner. HepG2 recovery was determined by the surface area covered by cells and growth factor concentration was measured to identify the factors involved in regeneration. Besides, HepG2 were collected for q-PCR analysis of injury, hepatocyte functional and regenerative markers expression. For the ADSCs, expression of hepatogenic differentiation genes was analyzed. Results showed that non-contact co-culture with ADSCs helped the recovery of injured HepG2. ELISA quantification revealed that ADSCs secreted higher amount of HGF and VEGF to help the recovery of injured HepG2. Furthermore, HepG2 co-cultured with ADSCs expressed significantly lower injury markers as well as significantly higher regenerative and functional markers compared to the control HepG2. ADSCs co-cultured with injured HepG2 expressed significantly higher hepatic related genes compared to the control ADSCs. In conclusion, ADSCs promote recovery of injured HepG2 via secretion of HGF and VEGF. In addition, co-cultured ADSCs showed early sign of hepatogenic differentiation in response to the factors released or secreted by the injured HepG2.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  16. Lee SH, Jaganath IB, Atiya N, Manikam R, Sekaran SD
    J Food Drug Anal, 2016 10;24(4):855-865.
    PMID: 28911625 DOI: 10.1016/j.jfda.2016.03.010
    Chemotherapies remain far from ideal due to drug resistance; therefore, novel chemotherapeutic agents with higher effectiveness are crucial. The extracts of four Phyllanthus species, namely Phyllanthus niruri, Phyllanthus urinaria, Phyllanthus watsonii, and Phyllanthus amarus, were shown to induce apoptosis and inhibit metastasis of breast carcinoma cells (MCF-7). The main objective of this study was to determine the pathways utilized by these four Phyllanthus species to exert anti-metastatic activities. A cancer 10-pathway reporter was used to investigate the pathways affected by the four Phyllanthus species. Results indicated that these Phyllanthus species suppressed breast carcinoma metastasis and proliferation by suppressing matrix metalloprotein 2 and 9 expression via inhibition of the extracellular signal-related kinase (ERK) pathway. Additionally, inhibition of hypoxia-inducible factor 1-α in the hypoxia pathway caused reduced vascular endothelial growth factor and inducible nitric oxide synthase expression, resulting in anti-angiogenic effects and eventually anti-metastasis. Two-dimensional gel electrophoresis identified numerous proteins suppressed by these Phyllanthus species, including invasion proteins, anti-apoptotic protein, protein-synthesis proteins, angiogenic and mobility proteins, and various glycolytic enzymes. Our results indicated that ERK and hypoxia pathways are the most likely targets of the four Phyllanthus species for the inhibition of MCF-7 metastasis.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  17. Bastion, M.L.C., Siti Aishah, S., Aida Zairani, M.Z., Barkeh, H.J.
    Medicine & Health, 2010;5(2):93-102.
    A retrospective case series review was conducted to determine the pre-operative role and safety of pre-operative adjunctive anti-vascular endothelial growth factor (anti- VEGF) agent ranibizumab “LUCENTISTM” in patients with diabetic retinopathy requiring vitrectomy. The study involved twenty consecutive eyes of sixteen patients (age range: 46-72 years; mean 57.5 years) which received intravitreal injection of 0.5 - 1 mg of ranibizumab 3 to 8 days (mean 4.4 days) prior to vitrectomy for diabetic retinopathy. There were no local or systemic post-injection complications. Indications for vitrectomy were retinal detachment (RD) [n=11; 3 combined tractional (TRD) - rhegmatogenous RD (RRD), 8 TRD], TRD with vitreous haemorrhage (VH) (n=3) ,VH (n=8) and vitreomacular traction syndrome (n=1). Inclusion criteria include all consecutive eyes of diabetic patients requiring vitrectomy receiving a first pre-operative injection of anti- VEGF. Pre-operative visual acuity (VA) ranged from 6/36 to light perception. All eyes had minimal to moderate intraoperative bleeding. Post-operative VH in eyes without tamponade or gas tamponade was nil (n=1), mild (n=13) or moderate (n=1). Silicone filled eyes had nil (n=1), moderate (n=3) or severe haemorrhages (n=1). Post-operative VA was unchanged (n=2) (10%), improved (n = 14) (70%) or worsened (n=4). VA was 2/60 or better (n=15) to no light perception (n=1). Two eyes achieved 6/12 or better vision (10%). Ten eyes (50%) had 6/36 or better vision. In conclusion, pre-operative intravitreal ranibizumab is safe and useful in diabetic vitrectomy and appears to help with perioperative bleeding leading to improvement in vision.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  18. Nur Aqilah, S., Wong, H.S., Syed Zulkifli, S.Z., Mushawiahti, M.
    Medicine & Health, 2018;13(1):88-96.
    Anti-vascular endothelial growth factor (VEGF) reduces choroidal thickness by choroidal hypoperfusion in diabetic macula oedema (DME) patients. Indirect effect of anti-VEGF towards outer retinal layers (ORL) which supplied by choroidal circulation has not been well described. We evaluate the ORL thickness between retinal pigment epithelium (RPE) with inner-segment-outer-segment photoreceptor junction (IS/OS) and RPE with external limiting membrane (ELM) in pre- and postintravitreal Ranibizumab (IVR) treated eyes with central foveal diabetic macula edema. A total of 60 eyes (40 patients) were analysed. ORL thickness measured with optical coherence tomography at pre- and post-injection day 1, week 4 and week 6. Mean thickness of RPE-IS/OS was statistically significant over time (p=0.023) but not for RPE-ELM (p=0.216). Thickness ratio between RPE-IS/OS and RPE-ELM and central subfoveal thickness (CST) both showed statistically significant result over time with p=0.038 and p=0.000, respectively. We observed an initial reduction of ORL thickness at day 1 followed by increased in thickness at week 4 with subsequent reduction at week 6 was observed. ORL is an aspect that can be explore and emphasized further in patients considered for IVR injections. The long-term effects of IVR to the ORL however could not be concluded due to short follow up period.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  19. Topchii II, Kirienko AN, Kirienko DA, Yakovtsova II, Gavriluk AA, Danyliuk SV, et al.
    Wiad. Lek., 2019;72(7):1269-1273.
    PMID: 31398154
    OBJECTIVE: Introduction: Vascular endothelium function interruption has the main role among mechanisms of development and progression of chronic kidney disease. In numerous experimental and clinical studies, it was proved that activated vascular endothelium is a structural and functional unit that matches processes of inflammation with intravascular coagulation, fibrinolysis and haemorheological disorders. The aim: To identify special features of endothelium morphological structure in kidney vessels, coronary arteries and aorta during chronic kidney disease.

    PATIENTS AND METHODS: Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used.

    RESULTS: Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwentprofound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.

    Matched MeSH terms: Vascular Endothelial Growth Factor A
  20. Lau TP, Roslani AC, Lian LH, Lee PC, Hilmi I, Goh KL, et al.
    Genet. Mol. Res., 2014;13(3):5555-61.
    PMID: 25117311 DOI: 10.4238/2014.July.25.9
    Growth factors are polypeptides that are critical for the initiation, progression, and metastasis of cancer. Most tumor cells are capable of synthesizing particular growth factors leading to constitutive pathway activation in these cells through autocrine signaling. Epidermal growth factor (EGF) is a potent mitogenic peptide that exerts direct effects on the proliferation and differentiation of tumor cells in carcinogenesis. By contrast, vascular endothelial growth factor (VEGF) is vital for the invasion and metastasis of neoplasms through the formation of new blood vessels from mature endothelial cells. In this study, we investigated the association between functional polymorphisms of both the EGF and VEGF genes and colorectal cancer (CRC) susceptibility. A total of 130 CRC patients and 212 healthy controls were recruited for this case-control study. Genotyping of genetic variants was conducted via real-time polymerase chain reaction (PCR) amplification with allele-specific TaqMan probes. None of the genotypes of the EGF +61 A>G and VEGF +936 C>T variants was significantly associated with CRC susceptibility among the Malaysian subjects evaluated (P > 0.05). The observed frequency distributions of the EGF +61 A>G polymorphism genotypes showed ethnic heterogeneity, which was not the case for the VEGF +936 C>T genotypes. In conclusion, no positive correlation between these functional polymorphisms and CRC risk was found in this Malaysian population. Studies of the EGF and VEGF genes and CRC susceptibility are scarce, and the results reported thus far differ from one population to another. Hence, more replication studies are warranted before any firm conclusions can be made.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/genetics*
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