scholarly journals Thrombospondin-1 differentially induces chemotaxis and DNA synthesis of human venous smooth muscle cells at the receptor-binding level

2002 ◽  
Vol 115 (22) ◽  
pp. 4353-4360 ◽  
Author(s):  
J. S. Lymn
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Receptor Binding ◽  
Muscle Cells ◽  
Thrombospondin 1 ◽  
Binding Level

Thrombospondin-1 Induces DNA Synthesis And Migration In Human Vascular Smooth Muscle Cells

1996 ◽  
Vol 24 (3) ◽  
pp. 446S-446S ◽  
Author(s):  
MAHENDRA K. PATEL ◽  
GERARD F. CLUNN ◽  
JOANNE S. LYMN ◽  
ALUN D. HUGHES
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Thrombospondin 1 ◽  
And Migration

Autocrine Induction of DNA Synthesis by Mechanical Injury of Cultured Smooth Muscle Cells

1996 ◽  
Vol 16 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Federico Calara ◽  
Sean Ameli ◽  
Anna Hultgårdh-Nilsson ◽  
Bojan Cercek ◽  
Joel Kupfer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Mechanical Injury ◽  
Cultured Smooth Muscle Cells

Fatty acid inhibition of angiotensin II-stimulated inositol phosphates in smooth muscle cells

1993 ◽  
Vol 264 (2) ◽  
pp. H595-H603
Author(s):  
M. E. Ullian
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Receptor Binding ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Muscle Cells ◽  
Ang Ii ◽  
Guanine Nucleotide Binding Protein ◽  
Cellular Incorporation

Inositol phosphate (InsP) responses to angiotensin II (ANG II) stimulation were measured in cultured rat vascular smooth muscle cells (VSMC) incubated with and without fatty acids (FA). VSMC were washed after 24 h of FA incubation to achieve cellular incorporation of FA yet eliminate ambient FA. Incubation with eicosapentaenoic acid (EPA)-supplemented medium resulted in concentration-dependent incorporation of EPA and depletion of arachidonic acid in VSMC membranes. Incubation with EPA, but not other FA, resulted in inhibition of ANG II-stimulated InsP formation (29% inhibition with 100 microM EPA). In contrast, InsP formation in response to guanine nucleotide-binding protein stimulation was not affected by EPA. ANG II receptor binding to membranes prepared from EPA-loaded VSMC was 18% lower than binding in membranes from sham-loaded cells. In other studies, VSMC were exposed acutely to FA to avoid cellular incorporation. Exposure to all FA resulted in concentration-dependent reductions in ANG II binding and ANG II-stimulated InsP formation; binding affinity was reduced without changes in receptor density. We conclude that ANG II-stimulated InsP formation is modestly and selectively inhibited by EPA incorporation and more profoundly inhibited by acute exposure to many FA via interference with ANG II receptor binding.

PDGF-BB-induced DNA synthesis is delayed by angiotensin II in vascular smooth muscle cells

1998 ◽  
Vol 274 (5) ◽  
pp. H1742-H1748 ◽  
Author(s):  
Gunilla Dahlfors ◽  
Yun Chen ◽  
Maria Wasteson ◽  
Hans J. Arnqvist
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Receptor Antagonist ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Β Receptor ◽  
Tgf Β1

The interaction of ANG II with platelet-derived growth factor (PDGF)-BB-induced DNA synthesis was studied in cultured rat aortic smooth muscle cells. PDGF-BB-induced DNA synthesis was delayed (∼6–8 h) by ANG II as shown by a time-course experiment. Losartan, an AT1-receptor antagonist, blocked the transient inhibitory effect of ANG II, whereas the AT2-receptor antagonist PD-123319 had no effect. Autocrine- or paracrine-acting transforming growth factor-β1 (TGF-β1), believed to be a mediator of ANG II-induced inhibitory effects, was not responsible for the delay of PDGF-BB-induced DNA synthesis, because a potent TGF-β1 neutralizing antibody could not reverse this effect of ANG II, nor was the delay of the PDGF-BB effect caused by inhibition of PDGF-β-receptor phosphorylation as shown by Western blot analysis of immunoprecipitated PDGF-β receptor. In conclusion, our results show that ANG II can exert a transient inhibitory effect on PDGF-BB-induced proliferation via the AT1 receptor.

Cyclic stretch activates p38 SAPK2-, ErbB2-, and AT1-dependent signaling in bladder smooth muscle cells

2000 ◽  
Vol 279 (4) ◽  
pp. C1155-C1167 ◽  
Author(s):  
Hiep T. Nguyen ◽  
Rosalyn M. Adam ◽  
Samuel H. Bride ◽  
John M. Park ◽  
Craig A. Peters ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Mapk Pathway ◽  
Muscle Cells ◽  
Cyclic Stretch ◽  
Bladder Smooth Muscle ◽  
Erk Mapk

Cyclic mechanical stretch of bladder smooth muscle cells (SMC) increases rates of DNA synthesis and stimulates transcription of the gene for heparin-binding epidermal growth factor-like growth factor (HB-EGF), an ErbB1/EGF receptor ligand that has been linked to hypertrophic bladder growth. In this study we sought to clarify the signaling pathways responsible for mechanotransduction of the stretch stimulus. HB-EGF mRNA levels, DNA synthesis, and AP-1/Ets DNA binding activities were induced by repetitive stretch of primary culture rat bladder SMC. Inhibitors of the p38 SAPK2 pathway, the angiotensin receptor type 1 (AT1), and the ErbB2 tyrosine kinase reduced each of these activities, while an inhibitor of the extracellular signal-regulated kinase mitogen-activated protein kinase (Erk-MAPK) pathway had no effect. Stretch rapidly activated stress-activated protein kinase 2 (p38 SAPK2) and Jun NH2-terminal kinase (JNK)/SAPK pathways but not the Erk-MAPK pathway and induced ErbB2 but not ErbB1 phosphorylation. Angiotensin II (ANG II) a bladder SMC mitogen previously linked to the stretch response, did not activate ErbB2, and ErbB2 activation occurred in response to stretch in the presence of an ANG receptor inhibitor, indicating that activation of the AT1-mediated pathway and the ErbB2-dependent pathway occurs by independent mechanisms. p38 SAPK2 and JNK/SAPK signaling also appeared to be independent of the ErbB2 and AT1 pathways. These findings indicate that stretch-stimulated DNA synthesis and gene expression in normal bladder SMC occur via multiple independent receptor systems (e.g., AT1 and ErbB2) and at least one MAPK pathway (p38 SAPK2). Further, we show that the Erk-MAPK pathway, which in most systems is linked to receptor-dependent cell growth responses, is not involved in progression to DNA synthesis or in the response of the HB-EGF gene to mechanical forces.

Endogenous activation of c-myc expression and DNA synthesis in serum-starved neonatal rat smooth muscle cells

1993 ◽  
Vol 52 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Anna Hultgårdh-Nilsson ◽  
Ulla Krondahl ◽  
Wei-Qin Jiang ◽  
Jan Nilsson ◽  
Nils R. Ringertz
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Neonatal Rat
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