Divergent effects of 17-β-estradiol on human vascular smooth muscle and endothelial cell function diminishes TNF-α-induced neointima formation

2012 ◽  
Vol 420 (4) ◽  
pp. 828-833 ◽  
Author(s):  
Rungrat Nintasen ◽  
Kirsten Riches ◽  
Romana S. Mughal ◽  
Parnpen Viriyavejakul ◽  
Urai Chaisri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Cell Function ◽  
Neointima Formation ◽  
Endothelial Cell Function ◽  
Tnf Α

Functional and structural adaptation of the yak pulmonary circulation to residence at high altitude

1993 ◽  
Vol 74 (5) ◽  
pp. 2276-2285 ◽  
Author(s):  
A. G. Durmowicz ◽  
S. Hofmeister ◽  
T. K. Kadyraliev ◽  
A. A. Aldashev ◽  
K. R. Stenmark
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
High Altitude ◽  
Pulmonary Circulation ◽  
Vascular Reactivity ◽  
Cell Function ◽  
Pulmonary Arteries ◽  
Structural Adaptation ◽  
Endothelial Cell Function

The high-altitude (HA) native yak (Bos grunniens) has successfully adapted to chronic hypoxia (CH) despite being in the same genus as domestic cows, which are known for their great hypoxic pulmonary vasoconstrictor responses (HPVRs), muscular pulmonary arteries, and development of severe pulmonary hypertension on exposure to CH. To determine possible mechanisms by which the pulmonary circulation may adapt to CH, yak pulmonary vascular reactivity to both vasoconstrictor and vasodilator stimuli and yak pulmonary artery structure were assessed. Hypoxia caused a small but significant HPVR, and norepinephrine infusion caused a greater rise in pulmonary arterial pressure (Ppa) than did hypoxia. Acetylcholine, an endothelium-dependent vasodilator, had no effect on Ppa but lowered pulmonary resistance (Rp) by causing an increase in cardiac output. Sodium nitroprusside, an endothelium-independent vasodilator, decreased both Ppa and Rp significantly. Yak small pulmonary arteries had a 4.1 +/- 0.1% medial thickness, with vessels < or = 100 microns devoid of smooth muscle. Yak pulmonary artery endothelial cells were much longer, wider, and rounder in appearance than those of domestic cows. Thus the yak has successfully adapted to HA conditions by maintaining both a blunted HPVR and thin-walled pulmonary vessels. Differences in both endothelial cell morphology and response to acetylcholine between the yak and those reported in the domestic cow suggest the adaptation to HA may include changes not only in the amount of pulmonary vascular smooth muscle but in endothelial cell function and structure as well.

scholarly journals A fibronectin-fibrinogen-tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function

2012 ◽  
Vol 16 (9) ◽  
pp. 2117-2126 ◽  
Author(s):  
Claudia Tersteeg ◽  
Mark Roest ◽  
Elske M. Mak-Nienhuis ◽  
Erik Ligtenberg ◽  
Imo E. Hoefer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Function ◽  
Endothelial Cell Function ◽  
Smooth Muscle Cell Growth

miRNA 146b-5p protects against atherosclerosis by inhibiting vascular smooth muscle cell proliferation and migration

Epigenomics ◽  
2020 ◽  
Author(s):  
Dating Sun ◽  
Gui Xiang ◽  
Jing Wang ◽  
Yuanyuan Li ◽  
Shuai Mei ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Function ◽  
Neointima Formation ◽  
And Migration ◽  
Aortic Plaques ◽  
Proliferation And Migration

Aim: To explore the potentially important role of miRNA 146b-5p (miR-146b) during the development of atherosclerosis. Materials & methods: Proliferation, migration and luciferase assays and mouse models were used to determine the functions of miR-146b. Results: miR-146b was identified as substantially upregulated in the aortic plaques of ApoE-/- mice as well as in response to inflammatory cytokines. Overexpression of miR-146b repressed proliferation and migration of vascular smooth muscle cells by downregulating Bag1 and Mmp16, respectively. Adeno-associated virus-mediated miR-146b overexpression inhibited neointima formation after carotid injury and suppressed atherosclerotic plaque formation in western diet-induced ApoE-/- mice. Conclusion: miR-146b is a novel regulator of vascular smooth muscle cell function induced by inflammatory response, specifically in neointima formation, and offers a novel therapeutic strategy for treating atherosclerosis.

Abstract 10: Endothelial FGF Protects Against Pulmonary Hypertension

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Kel Vin Woo ◽  
Carla Weinheimer ◽  
Attila Kovacs ◽  
David Ornitz
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Right Ventricular ◽  
Cell Function ◽  
Weight Ratio ◽  
Ventricular Pressure ◽  
Fibroblast Growth Factor Receptors ◽  
Endothelial Cell Function ◽  
The Impact

Pulmonary hypertension (PH) is a debilitating disease where 1 in 4 patients will die within five years of diagnosis. Pathologic changes of endothelial cell function, together with smooth muscle and adventitial hyperplasia increase pulmonary vascular resistance. Consequent elevation in right ventricular pressure ultimately causes right heart failure. Expression of Fibroblast Growth Factor Receptors (FGFRs), FGFR1 and FGFR2, are elevated in lung samples from PH patients; however, the impact of these receptors on endothelial cell function, and endothelial to smooth muscle interaction is poorly understood. We hypothesize that activation of endothelial FGFR1 and FGFR2 promotes endothelial cell survival, elaborating signals that protect against pulmonary hypertension via inhibition of smooth muscle cell recruitment. We used the Tie2-Cre transgene to conditionally inactivate Fgfr1 and Fgfr2 in endothelial cells. Experimental mice with genotype Tie2-Cre; Fgfr1 f/f ; Fgfr2 f/f (DCKO) and control Fgfr1 f/f ; Fgfr2 f/f (DFF) were challenged with 10% hypoxia for 2 weeks. At the end, right ventricular pressure (RVp) was measured by cardiac catheterization. Compared to mice in normoxia, control littermates in hypoxia demonstrated significant increases in RVp, and RV to left ventricle + septum (LV+S) weight ratio, consistent with development of PH. DCKO mice demonstrate further elevation in RVp and an increase in the RV to LV+S weight ratio, demonstrating worsening PH. We also observed formation of plexiform lesions in DCKO mice, suggestive of a severe pathology. We found a previously unreported involvement of FGF10 in pulmonary hypertension. FGF10 expression was decreased in hypoxia-challenged DCKO mice as compared to both DCKO littermates on room air, and to hypoxia challenged DFF control mice. Our data suggests that endothelial FGFR1 and FGFR2 activation may protect against pulmonary hypertension. Further studies are underway to elucidate the role of FGF10 and its mechanism in the pathology. We will also further identify associated FGF ligands, associated signaling mechanisms, and endothelial to smooth muscle interactions.

Thrombin, TNF-α, and LPS exert overlapping but nonidentical effects on gene expression in endothelial cells and vascular smooth muscle cells

2005 ◽  
Vol 289 (2) ◽  
pp. H873-H885 ◽  
Author(s):  
Sheng-Qian Wu ◽  
William C. Aird
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Cell Activation ◽  
Expression Profiles ◽  
Critical Role ◽  
Cell Type ◽  
Endothelial Cell Activation ◽  
Tnf Α

Thrombin, TNF-α, and LPS have each been implicated in endothelial cell and vascular smooth muscle cell (VSMC) activation. We wanted to test the hypothesis that these three agonists display mediator and/or cell type-specific properties. The addition of thrombin to human pulmonary artery endothelial cells resulted in an upregulation of PDGF-A, tissue factor (TF), ICAM-1, and urokinase-type plasminogen activator (u-PA), whereas TNF-α and LPS failed to induce PDGF-A. These effects were mimicked by protease-activated receptor-1 activation. In VSMC, thrombin induced expression of TF and PDGF-A but failed to consistently induce ICAM-1 or u-PA expression. In contrast, TNF-α and LPS increased expression of all four genes in this cell type. Inhibitor studies in endothelial cells demonstrated a critical role for PKC in mediating thrombin, TNF-α, and LPS induction of ICAM-1, TF, and u-PA and for p38 MAPK in mediating thrombin, TNF-α, and LPS induction of TF. Taken together, these results suggest that inflammatory mediators engage distinct signaling pathways and expression profiles in endothelial cells and VSMC. The data support the notion that endothelial cell activation is not an all-or-nothing phenomenon but rather is dependent on the nature of the extracellular mediator.

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