scholarly journals Exploring the Mechanism of Microarteriogenesis in Porous Silk Fibroin Film

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Lun Bai ◽  
Guangqian Wang ◽  
Xiaoyan Tan ◽  
Jianmei Xu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Silk Fibroin ◽  
Muscle Cell ◽  
Tissue Repair ◽  
Repair Process ◽  
Sd Rats ◽  
Silk Fibroin Film ◽  
Capillary Angiogenesis

Purpose. Based on the experiment of the microarteriogenesis that is associated with angiogenesis during tissue repair process in porous silk fibroin films (PSFFs), we investigate the characteristics of micro-arteriogenesis and explore its mechanism.Methods. After the porous silk fibroin materials are implanted into the back hypodermal tissue of SD rats, the arteriole development and the morphogenesis of smooth muscle cell are histologically monitored and the micro-arteriogenesis is quantitatively analyzed.Results. 10 days after implantation, the arteriole density reaches the highest level in the junction of silk fibroin materials with tissues. Three weeks later, the arteriolar density in the materials reaches the maximum, and the arterioles in the junction of materials with tissues appear to be in a mature and upgrading state.Modeling of Microarteriogenesis. The arterioles in materials are generated after capillary angiogenesis. It is inferred that arteriolar development does not start until the network of the capillaries is formed. At first, the arterioles grow in the conjunct area of precapillaries with arterioles. Then with the extension of the arterioles, the upgrade of arterioles in connecting area is observed at a later stage. Based on the observation, the conditions and the mechanism of microarterializations as well as the upgrade of arterioles are analyzed.

scholarly journals Electrospun silk fibroin/poly (L-lactide-ε-caplacton) graft with platelet-rich growth factor for inducing smooth muscle cell growth and infiltration

2016 ◽  
Vol 3 (4) ◽  
pp. 239-245 ◽  
Author(s):  
Anlin Yin ◽  
Gary L. Bowlin ◽  
Rifang Luo ◽  
Xingdong Zhang ◽  
Yunbing Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Cell Growth ◽  
Smooth Muscle Cell ◽  
Silk Fibroin ◽  
Muscle Cell ◽  
Smooth Muscle Cell Growth

1429: Upregulation of Rho-Kinase in a Human Corpus Cavernosum Smooth Muscle Cell Line in Response to Hypoxia

2004 ◽  
Vol 171 (4S) ◽  
pp. 376-377
Author(s):  
Yongmu Zheng ◽  
Shaohua Chang ◽  
Alan J. Wein ◽  
Samuel Chacko ◽  
Michael E. DiSanto
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Line ◽  
Muscle Cell ◽  
Corpus Cavernosum ◽  
Rho Kinase ◽  
Muscle Cell Line

Involvement of Cyclooxygenase- and Lipoxygenase-Mediated Conversion of Arachidonic Acid in Controlling Human Vascular Smooth Muscle Cell Proliferation

1990 ◽  
Vol 63 (02) ◽  
pp. 291-297 ◽  
Author(s):  
Herm-Jan M Brinkman ◽  
Marijke F van Buul-Worteiboer ◽  
Jan A van Mourik
Keyword(s):  
Cell Proliferation ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Muscle Cells ◽  
Smooth Muscle Cell Proliferation

SummaryWe observed that the growth of human umbilical arterysmooth muscle cells was inhibited by the phospholipase A2 inhibitors p-bromophenacylbromide and mepacrine. Thesefindings suggest that fatty acid metabolism might be integrated in the control mechanism of vascular smooth muscle cell proliferation. To identify eicosanoids possibly involved in this process, we studied both the metabolism of arachidonic acid of these cells in more detail and the effect of certain arachidonic acid metabolites on smooth muscle cells growth. We found no evidence for the conversion of arachidonic acid via the lipoxygenase pathway. In contrast, arachidonic acid was rapidly converted via the cyclooxy-genase pathway. The following metabolites were identified: prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-k-PGF1α), prostaglandin F2α (PGF2α), 12-hydroxyheptadecatrienoic acid (12-HHT) and 11-hydroxyeicosatetetraenoic acid (11-HETE). PGE2 was the major metabolite detected. Arachidonic acid metabolites were only found in the culture medium, not in the cell. After synthesis, 11-HETE was cleared from the culture medium. We have previously reported that PGE2 inhibits the serum-induced [3H]-thymidine incorporation of growth-arrested human umbilical artery smooth muscle cells. Here we show that also 11-HETEexerts this inhibitory property. Thus, our data suggeststhat human umbilical artery smooth muscle cells convert arachidonic acid only via the cyclooxygenase pathway. Certain metabolites produced by this pathway, including PGE2 and 11-HETE, may inhibit vascular smooth muscle cell proliferation.

The Migration of Human Smooth Muscle Cells In Vitro Is Mediated by Plasminogen Activation and Can Be Inhibited by α2-Macroglobulin Receptor Associated Protein

1997 ◽  
Vol 78 (02) ◽  
pp. 880-886 ◽  
Author(s):  
Monique J Wijnberg ◽  
Paul H A Quax ◽  
Nancy M E Nieuwenbroek ◽  
Jan H Verheijen
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Ldl Receptor ◽  
Migration And Invasion ◽  
Invasion Assay ◽  
Plasminogen Activation ◽  
Smooth Muscle Cell Migration

SummaryThe plasminogen activation system is thought to be important in cell migration processes. A role for this system during smooth muscle cell migration after vascular injury has been suggested from several animal studies. However, not much is known about its involvement in human vascular remodelling. We studied the involvement of the plasminogen activation system in human smooth muscle cell migration in more detail using an in vitro wound assay and a matrix invasion assay. Inhibition of plasmin activity or inhibition of urokinase-type plasminogen activator (u-PA) activity resulted in approximately 40% reduction of migration after 24 h in the wound assay and an even stronger reduction (70-80%) in the matrix invasion assay. Migration of smooth muscle cells in the presence of inhibitory antibodies against tissue-type plasminogen activator (t-PA) was not significantly reduced after 24 h, but after 48 h a 30% reduction of migration was observed, whereas in the matrix invasion assay a 50% reduction in invasion was observed already after 24 h. Prevention of the interaction of u-PA with cell surface receptors by addition of soluble u-PA receptor or α2-macroglobulin receptor associated protein (RAP) to the culture medium, resulted in a similar inhibition of migration and invasion. From these results it can be concluded that both u-PA and t-PA mediated plasminogen activation can contribute to in vitro human smooth muscle cell migration and invasion. Furthermore, the interaction between u-PA and its cell surface receptor appears also to be involved in this migration and invasion process. The inhibitory effects on migration and invasion by the addition of RAP suggests an involvement of a RAP sensitive receptor of the LDL receptor family, possibly the LDL-receptor related protein (LRP) and/or the VLDL receptor.

Sign in / Sign up

Export Citation Format

Share Document