Document Detail


Mechanisms related to NO-induced motility in differentiated rat aortic smooth muscle cells.
MedLine Citation:
PMID:  21037226     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nitric oxide (NO) is thought to play an important role as an inhibitor of vascular cell proliferation, motility, and neointima formation. This effect is mediated, in part, via the upregulation of protein tyrosine phosphatase (PTP)1B. Conversely, studies have reported that in presumably hyperinsulinemic mice fed a high-fat diet, NO enhances vascular remodeling, whereas a deficit of NO attenuates vascular remodeling. We have reported that in differentiated cultured smooth muscle cells treated with insulin, NO induces a motogenic effect that is dependent on Src homology-2 domain PTP 2 (SHP2) upregulation. In the present study, we describe novel mechanisms relevant to the motogenic effect of NO. Treatment of cultured cells with the selective angiontensin type 1 receptor antagonist losartan, but not with the selective angiotensin type 2 receptor antagonist PD-123319, blocked the comotogenic capacity of NO and insulin. Insulin and NO increased the secretion of ANG II into the culture media by 2- and 2.5-fold (P < 0.05), respectively, whereas treatment of cells with ANG II uncovered the motogenic effect of NO (1.4-fold above control, P < 0.05) and decreased the levels of PTP1B to 45% of control (P < 0.05). Suppression of PTP1B function was sufficient to uncover the motogenic effect of NO. The capacity of insulin to suppress PTP1B activity was blocked by losartan, implicating ANG II function in mediating this effect. Both insulin and ANG II induced the upregulation of phosphatidyl inositol 3-kinase (PI3K)-δ by two- to threefold (P < 0.05), and this effect was both necessary and sufficient to uncover NO-induced motogenesis. Finally, suppression of PTP1B function potentiated, whereas overexpression of PTP1B inhibited, SHP2-induced motogenesis. These results support the hypothesis that the comotogenic effect of insulin and NO occurs via an ANG II-mediated effect involving the suppression of PTP1B and upregulation of PI3K-δ and SHP2.
Authors:
Qinghua Pu; Daming Zhuang; Shalini Thakran; Aviv Hassid
Related Documents :
17911226 - Predicting beef tenderness using near-infrared spectroscopy.
2952496 - Impaired 6-phosphofructokinase activity in mononuclear leukocytes from patients with ty...
15087286 - Gender differences in ang ii levels and action on multiple k+ current modulation pathwa...
8466716 - Antihypertensive efficacy, safety, and tolerability of isradipine in hypertensive patie...
15663466 - Detection of single and mixed vocs by smell and by sensory irritation.
6732576 - Polyol pathway metabolites in human cataracts. correlation of circulating glycosylated ...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-29
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  300     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-04     Completed Date:  2011-01-28     Revised Date:  2012-01-02    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H101-8     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Angiotensin II / metabolism
Angiotensin II Type 1 Receptor Blockers / pharmacology
Angiotensin II Type 2 Receptor Blockers / pharmacology
Animals
Aorta, Thoracic / cytology,  drug effects,  metabolism*
Cell Movement / drug effects,  physiology*
Cells, Cultured
Enzyme-Linked Immunosorbent Assay
Imidazoles / pharmacology
Insulin / metabolism,  pharmacology*
Losartan / pharmacology
Male
Muscle, Smooth, Vascular / cytology,  drug effects,  metabolism*
Myocytes, Smooth Muscle / cytology,  drug effects,  metabolism*
Nitric Oxide / metabolism,  pharmacology*
Phosphatidylinositol 3-Kinases / metabolism
Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism
Pyridines / pharmacology
RNA, Small Interfering
Rats
Rats, Sprague-Dawley
Up-Regulation
Grant Support
ID/Acronym/Agency:
HL-63886/HL/NHLBI NIH HHS; HL-72902/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Angiotensin II Type 2 Receptor Blockers; 0/Imidazoles; 0/Insulin; 0/Pyridines; 0/RNA, Small Interfering; 10102-43-9/Nitric Oxide; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 130663-39-7/PD 123319; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 3.1.3.48/Protein Tyrosine Phosphatase, Non-Receptor Type 11

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killi...
Next Document:  Accurate estimation of entropy in very short physiological time series: the problem of atrial fibril...