scholarly journals Effects of 17β-Estradiol on the Plasminogen Activator System in Vascular Smooth Muscle Cells Treated with Lysophophatidylcholine

2020 ◽  
Vol 26 (1) ◽  
pp. 9
Author(s):  
Byung-Koo Yoon ◽  
Young-Hee Kang ◽  
Won-Jong Oh ◽  
Dong-Yun Lee ◽  
Duk-Kyung Kim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Plasminogen Activator System ◽  
17Β Estradiol ◽  
Activator System

Effects of black cohosh on the plasminogen activator system in vascular smooth muscle cells

Maturitas ◽  
2013 ◽  
Vol 76 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Dong-Yun Lee ◽  
Cheong-Rae Roh ◽  
Young-Hee Kang ◽  
DooSeok Choi ◽  
YoungJoo Lee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Black Cohosh ◽  
Plasminogen Activator System ◽  
Activator System

scholarly journals 17β-estradiol down-regulates lipopolysaccharide-induced MCP-1 production and cell migration in vascular smooth muscle cells

2010 ◽  
Vol 45 (2) ◽  
pp. 87-97 ◽  
Author(s):  
Ping Jiang ◽  
Jinwen Xu ◽  
Shuhui Zheng ◽  
Jinghe Huang ◽  
Qiuling Xiang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
P38 Mapk ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Pyrrolidine Dithiocarbamate ◽  
17Β Estradiol ◽  
Anti Inflammatory

Atherosclerosis is an inflammatory disease where lipopolysaccharide (LPS) triggers the release of inflammatory cytokines that accelerate its initiation and progression. Estrogen has been proven to be vasoprotective against atherosclerosis; however, the anti-inflammatory function of estrogen in the vascular system remains obscure. In this study, we investigated the effect of estrogen on LPS-induced monocyte chemoattractant protein-1 (MCP-1; listed as CCL2 in the MGI database) production in vascular smooth muscle cells (VSMCs). LPS significantly enhances MCP-1 production and this is dependent on nuclear factor κ B (NFκB) signaling, since the use of NFκB inhibitor pyrrolidine dithiocarbamate or the silencing of NFκB subunit p65 expression with specific siRNA largely impairs LPS-enhanced MCP-1 production. On the contrary, 17β-estradiol (E2) inhibits LPS-induced MCP-1 production in a time- and dose-dependent manner, which is related to the suppression of p65 translocation to nucleus. Furthermore, p38 MAPK is rapidly activated in response to LPS, while E2 markedly inhibits p38 MAPK activation. Transfection with p38 MAPK siRNA or the use of p38 MAPK inhibitor SB203580 markedly attenuates LPS-stimulated p65 translocation to nucleus and MCP-1 production, suggesting that E2 suppresses NFκB signaling by the inactivation of p38 MAPK signaling. LPS promotes VSMCs migration and this is abrogated by MCP-1 antibody, implying that MCP-1 may play a major role as an autocrine factor in atherosclerosis. In addition, E2 inhibits LPS-promoted cell migration by downregulation of MCP-1 production. Overall, our results demonstrate that E2 exerts anti-inflammatory property antagonistic to LPS in VSMCs by reducing MCP-1 production, and this effect is related to the inhibition of p38 MAPK/NFκB cascade.

LRP and αvβ3 mediate tPA activation of smooth muscle cells

2006 ◽  
Vol 291 (3) ◽  
pp. H1351-H1359 ◽  
Author(s):  
Sa'ed Akkawi ◽  
Taher Nassar ◽  
Mark Tarshis ◽  
Douglas B. Cines ◽  
Abd Al-Roof Higazi
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Vascular Smooth Muscle Cells ◽  
Density Lipoprotein ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Tissue Type ◽  
Pai 1

Tissue-type plasminogen activator (tPA) regulates vascular contractility through the low-density lipoprotein-related receptor (LRP), and this effect is inhibited by plasminogen activator inhibitor type 1 (PAI-1). We now report that tPA-mediated vasocontraction also requires the integrin αvβ3. tPA-induced contraction of rat aortic rings is inhibited by the Arg-Gly-Asp (RGD) peptide and by monoclonal anti-αvβ3 antibody. tPA induces the formation of a complex between LRP and αvβ3 in vascular smooth muscle cells. The three proteins are internalized within 10 min, causing the cells to become refractory to the readdition of tPA. LRP and αvβ3 return to the cell surface by 90 min, restoring cell responsiveness to tPA. PAI-1 and the PAI-1-derived hexapeptide EEIIMD abolish the vasocontractile activity of tPA and inhibit the tPA-mediated interaction between LRP and αvβ3. tPA induces calcium mobilization from intracellular stores in vascular smooth muscle cells, and this effect is inhibited by PAI-1, RGD, and antibodies to both LRP and αvβ3. These data indicate that tPA-mediated vasocontraction involves the coordinated interaction of LRP with αvβ3. Delineating the mechanism underlying these interactions and the nature of the signals transduced may provide new tools to regulate vascular tone and other consequences of tPA-mediated signaling.

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