T Cell—Vascular Smooth Muscle Cell Interactions: Antigen-Specific Activation and Cell Cycle Blockade of T Helper Clones by Cloned Vascular Smooth Muscle Cells

1995 ◽  
Vol 218 (1) ◽  
pp. 331-338 ◽  
Author(s):  
Jill Suttles ◽  
Robert W. Miller ◽  
Carolyn F. Moyer
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
T Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
T Helper

scholarly journals Morphogenesis and differentiation of embryonic vascular smooth muscle cells in zebrafish

2018 ◽  
Author(s):  
Thomas R. Whitesell ◽  
Paul Chrystal ◽  
Jae-Ryeon Ryu ◽  
Nicole Munsie ◽  
Ann Grosse ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Critical Role ◽  
Muscle Cells ◽  
Mural Cells

AbstractDespite the critical role of vascular mural cells (smooth muscle cells and pericytes) in supporting the endothelium of blood vessels, we know little of their early morphogenesis and differentiation. foxc1b:EGFP expressing cells in zebrafish associate with the vascular endothelium (kdrl) and co-express a smooth muscle marker (acta2), but not a pericyte marker (pdgfrβ). The expression of foxc1b in early peri-endothelial mesenchymal cells allows us to follow the morphogenesis of mesenchyme into acta2 expressing vascular smooth muscle cells. We show that mural cells expressing different markers associate with vessels of different diameters, depending on their embryonic location and developmental timing, suggesting marker expression is predictive of functional differences. We identify gene expression signatures for an enriched vascular smooth muscle cell population (foxc1b + acta2) and all smooth muscle (acta2) using fluorescence-activated cell sorting and RNA-Seq. Finally, we demonstrate that progressive loss of foxc1a/foxc1b results in decreased smooth muscle cell coverage. Together, our data highlight the early cellular dynamics and transcriptome profiles of smooth muscle cells in vivo, using foxc1b as a unique tool to probe vascular smooth muscle cell differentiation.Summary StatementTracing the morphogenesis and transcriptome of early vascular smooth muscle cells using foxc1b

Heparin inhibits Na(+)-H+ exchange in vascular smooth muscle cells

1990 ◽  
Vol 258 (1) ◽  
pp. C46-C53 ◽  
Author(s):  
R. Zaragoza ◽  
K. M. Battle-Tracy ◽  
N. E. Owen
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Muscle Cells

Vascular smooth muscle cell proliferation has been shown to be an important factor in atheromatous plaque formation, hypertrophy associated with essential hypertension, and failure of balloon angioplasty procedures. Investigators have shown that a number of different agents stimulate vascular smooth muscle cell proliferation, including epidermal growth factor, platelet-derived growth factor, angiotensin II, and catecholamines. Previously, we have demonstrated that these agents also cause immediate changes in ion transport and second messenger generation in vascular smooth muscle cells. We have proposed that these immediate changes may be linked to each other and to cell proliferation. In contrast to the many agents that have been shown to stimulate vascular smooth muscle cell proliferation, only a few agents (e.g., heparin sodium or transforming growth factor-beta) have been shown to inhibit vascular smooth muscle cell proliferation. In the present study we have investigated whether heparin inhibits serum- or growth factor-stimulated changes in ion transport and second messenger generation in vascular smooth muscle cells. We found that heparin inhibits serum- or growth factor-stimulated Na(+)-H+ exchange in a concentration-dependent manner that is not dependent on the ability of heparin to function as an anticoagulant agent. In addition, other glycosaminoglycans were not found to be inhibitory, and the inhibitory effects of heparin were discovered to be limited to vascular smooth muscle cells. Heparin does not appear to be acting by binding to growth factors, or by directly inhibiting the Na(+)-H+ exchange protein. However, heparin did inhibit serum- or growth factor-stimulated inositol trisphosphate release and calcium mobilization.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Increased vascular smooth muscle cell stiffness: a novel mechanism for aortic stiffness in hypertension

2013 ◽  
Vol 305 (9) ◽  
pp. H1281-H1287 ◽  
Author(s):  
Nancy L. Sehgel ◽  
Yi Zhu ◽  
Zhe Sun ◽  
Jerome P. Trzeciakowski ◽  
Zhongkui Hong ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Muscle Cells ◽  
Vascular Stiffness ◽  
Cell Stiffness

Increased vascular stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular stiffness in hypertension only involve the extracellular matrix and endothelium. We hypothesized that increased large-artery stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle cells. After confirming increased arterial pressure and aortic stiffness in spontaneously hypertensive rats, we found increased elastic stiffness of aortic smooth muscle cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the stiffness of vascular smooth muscle cells derived from hypertensive and control rats, suggesting that a dynamic component to cellular elastic stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle cell cytoskeletal proteins reduced vascular smooth muscle cell stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that stiffness of individual vascular smooth muscle cells mediates vascular stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular stiffness.

scholarly journals Cellular action and interactions of arginine vasopressin in vascular smooth muscle: mechanisms and clinical implications.

1993 ◽  
Vol 4 (1) ◽  
pp. 2-11
Author(s):  
R W Schrier ◽  
V Briner ◽  
C Caramelo
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Arginine Vasopressin ◽  
Clinical Implications ◽  
Mitogenic Effect

In recent years, much has been learned about the vascular action of arginine vasopressin (AVP) including (1) the structure, internalization, and recycling of the V1 AVP receptor; (2) the AVP postreceptor signaling events for the initial and sustained vascular smooth muscle cell contraction as well as the hormone's mitogenic effect; (3) the process of homologous and heterologous AVP desensitization in vascular smooth muscle cells; (4) the interaction of AVP with other vasoconstrictor and vasodilator hormones; (5) the vascular interaction of AVP with endothelial events; and (6) the vascular interactions that may occur with systemic acidemia or alkalemia as well as with ethanol. The various potential clinical and biochemical implications of these results are discussed briefly.

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.

Sign in / Sign up

Export Citation Format

Share Document