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Fulltext Human adipose tissue derived stem cells as a source of smooth muscle cells in the regeneration of muscular layer of urinary bladder wall

Salem SA, Hwie AN, Saim A, Chee Kong CH, Sagap I, Singh R, et al.

Malays J Med Sci, 2013 Jul;20(4):80-7.
PMID: 24044001 MyJurnal

Adipose tissue provides an abundant source of multipotent cells, which represent a source of cell-based regeneration strategies for urinary bladder smooth muscle repair. Our objective was to confirm that adipose-derived stem cells (ADSCs) can be differentiated into smooth muscle cells.

Matched MeSH terms: Myocytes, Smooth Muscle
In vitro and in vivo degradation evaluation of novel iron-bioceramic composites for bone implant applications

Ulum MF, Arafat A, Noviana D, Yusop AH, Nasution AK, Abdul Kadir MR, et al.

Mater Sci Eng C Mater Biol Appl, 2014 Mar 1;36:336-44.
PMID: 24433920 DOI: 10.1016/j.msec.2013.12.022

Biodegradable metals such as magnesium, iron and their alloys have been known as potential materials for temporary medical implants. However, most of the studies on biodegradable metals have been focusing on optimizing their mechanical properties and degradation behavior with no emphasis on improving their bioactivity behavior. We therefore investigated the possibility of improving iron biodegradation rate and bioactivity by incorporating various bioactive bioceramics. The iron-based bioceramic (hydroxyapatite, tricalcium phosphate and biphasic calcium phosphate) composites were prepared by mechanical mixing and sintering process. Degradation studies indicated that the addition of bioceramics lowered the corrosion potential of the composites and slightly increased their corrosion rate compared to that of pure iron. In vitro cytotoxicity results showed an increase of cellular activity when rat smooth muscle cells interacted with the degrading composites compared to pure iron. X-ray radiogram analysis showed a consistent degradation progress with that found in vivo and positive tissue response up to 70 days implantation in sheep animal model. Therefore, the iron-based bioceramic composites have the potential to be used for biodegradable bone implant applications.

Matched MeSH terms: Myocytes, Smooth Muscle/cytology; Myocytes, Smooth Muscle/drug effects
Microfluidic production of bioactive fibrin micro-beads embedded in crosslinked collagen used as an injectable bulking agent for urinary incontinence treatment

Vardar E, Larsson HM, Allazetta S, Engelhardt EM, Pinnagoda K, Vythilingam G, et al.

Acta Biomater, 2018 02;67:156-166.
PMID: 29197579 DOI: 10.1016/j.actbio.2017.11.034

Endoscopic injection of bulking agents has been widely used to treat urinary incontinence, often due to urethral sphincter complex insufficiency. The aim of the study was to develop a novel injectable bioactive collagen-fibrin bulking agent restoring long-term continence by functional muscle tissue regeneration. Fibrin micro-beads were engineered using a droplet microfluidic system. They had an average diameter of 140 μm and recombinant fibrin-binding insulin-like growth factor-1 (α2PI1-8-MMP-IGF-1) was covalently conjugated to the beads. A plasmin fibrin degradation assay showed that 72.5% of the initial amount of α2PI1-8-MMP-IGF-1 loaded into the micro-beads was retained within the fibrin micro-beads. In vitro, the growth factor modified fibrin micro-beads enhanced cell attachment and the migration of human urinary tract smooth muscle cells, however, no change of the cellular metabolic activity was seen. These bioactive micro-beads were mixed with genipin-crosslinked homogenized collagen, acting as a carrier. The collagen concentration, the degree of crosslinking, and the mechanical behavior of this bioactive collagen-fibrin injectable were comparable to reference samples. This novel injectable showed no burst release of the growth factor, had a positive effect on cell behavior and may therefore induce smooth muscle regeneration in vivo, necessary for the functional treatment of stress and other urinary incontinences.
STATEMENT OF SIGNIFICANCE: Urinary incontinence is involuntary urine leakage, resulting from a deficient function of the sphincter muscle complex. Yet there is no functional cure for this devastating condition using current treatment options. Applied physical and surgical therapies have limited success. In this study, a novel bioactive injectable bulking agent, triggering new muscle regeneration at the injection site, has been evaluated. This injectable consists of cross-linked collagen and fibrin micro-beads, functionalized with bound insulin-like growth factor-1 (α2PI1-8-MMP-IGF-1). These bioactive fibrin micro-beads induced human smooth muscle cell migration in vitro. Thus, this injectable bulking agent is apt to be a good candidate for regeneration of urethral sphincter muscle, ensuring a long-lasting treatment for urinary incontinence.

Matched MeSH terms: Myocytes, Smooth Muscle/metabolism; Myocytes, Smooth Muscle/pathology
Fulltext Morphology of the human aorta and age-related changes: anatomical facts

Komutrattananont P, Mahakkanukrauh P, Das S

Anat Cell Biol, 2019 Jun;52(2):109-114.
PMID: 31338225 DOI: 10.5115/acb.2019.52.2.109

Aorta is the largest artery in the human body. Its starting point is the aortic orifice of the aortic valve and it terminates at the level of the fourth lumbar vertebra. The main function of the aorta is to transport oxygenated blood to supply all the organs and cells. With advancing age, the structure and hence the function show progressive changes. Various changes in the aortic morphology include the luminal diameter of aorta, whole length of the aorta, thickness, the microstructural components also change, and these include collagen, elastin and smooth muscle cells. In addition, the dimensions of all segments of the aorta increase with age in both sexes. Since age is a major risk factor for degenerative change and diseases affecting the aorta, understanding the detailed anatomy of the aorta may provide essential information concerning the age-associated process of the aorta. Knowledge of the morphological changes in the aorta is also important for future clinical therapies pertaining to aortic disease. Additionally, the information regarding the structural changes with age may be applied for age determination. This review describes the overview of the anatomy of the aorta, age related changes in the morphology of the aorta and aortic diseases.

Matched MeSH terms: Myocytes, Smooth Muscle
Fulltext Inhibition of Egr1 expression underlies the anti-mitogenic effects of cAMP in vascular smooth muscle cells

Kimura TE, Duggirala A, Hindmarch CC, Hewer RC, Cui MZ, Newby AC, et al.

J Mol Cell Cardiol, 2014 Jul;72(100):9-19.
PMID: 24534707 DOI: 10.1016/j.yjmcc.2014.02.001

AIMS: Cyclic AMP inhibits vascular smooth muscle cell (VSMC) proliferation which is important in the aetiology of numerous vascular diseases. The anti-mitogenic properties of cAMP in VSMC are dependent on activation of protein kinase A (PKA) and exchange protein activated by cAMP (EPAC), but the mechanisms are unclear.
METHODS AND RESULTS: Selective agonists of PKA and EPAC synergistically inhibited Egr1 expression, which was essential for VSMC proliferation. Forskolin, adenosine, A2B receptor agonist BAY60-6583 and Cicaprost also inhibited Egr1 expression in VSMC but not in endothelial cells. Inhibition of Egr1 by cAMP was independent of cAMP response element binding protein (CREB) activity but dependent on inhibition of serum response element (SRE) activity. SRF binding to the Egr1 promoter was not modulated by cAMP stimulation. However, Egr1 expression was dependent on the SRF co-factors Elk1 and 4 but independent of MAL. Inhibition of SRE-dependent Egr1 expression was due to synergistic inhibition of Rac1 activity by PKA and EPAC, resulting in rapid cytoskeleton remodelling and nuclear export of ERK1/2. This was associated with de-phosphorylation of the SRF co-factor Elk1.
CONCLUSION: cAMP inhibits VSMC proliferation by rapidly inhibiting Egr1 expression. This occurs, at least in part, via inhibition of Rac1 activity leading to rapid actin-cytoskeleton remodelling, nuclear export of ERK1/2, impaired Elk1-phosphorylation and inhibition of SRE activity. This identifies one of the earliest mechanisms underlying the anti-mitogenic effects of cAMP in VSMC but not in endothelial cells, making it an attractive target for selective inhibition of VSMC proliferation.

Matched MeSH terms: Myocytes, Smooth Muscle/cytology; Myocytes, Smooth Muscle/drug effects; Myocytes, Smooth Muscle/metabolism*