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Arterial Smooth Muscle Cells (arterial + smooth_muscle_cell)
Selected AbstractsDecorin synthesized by arterial smooth muscle cells is retained in fibrin gels and modulates fibrin contractionJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2007Pamela Y. Johnson Abstract Fibrin serves as a provisional extracellular matrix (ECM) for arterial smooth muscle cells (ASMC) after vascular injury, yet little is known about the effect of fibrin on ECM remodeling by these cells. To address this question, monkey ASMC were grown on fibrin gels and tissue culture (TC) plastic, and proteoglycan synthesis and accumulation were assessed by radiolabeling. Initial rates of 35S-sulfate incorporation into proteoglycans were identical for both groups, but increased proteoglycan accumulation was observed in cultures grown for 48 h on fibrin. This increased accumulation on fibrin was due to reduced proteoglycan turnover and retention within the fibrin gel. Decorin and biglycan constituted 40 and 14% of the total proteoglycan in the fibrin gels, whereas their combined contribution was only 12% in control matrices. To explore whether the retention of decorin in fibrin had any influence on the properties of the fibrin gel, ASMC-mediated fibrin contraction assays were performed. Both de novo synthesis of decorin as well as decorin added during polymerization inhibited the ability of the cells to contract fibrin. In contrast, decorin added exogenously to mature fibrin matrices had no effect on fibrin gel contraction. This study illustrates that decorin derived from ASMC selectively accumulates in fibrin and modifies fibrin architecture and mechanical properties. Such an accumulation may influence wound healing and the thrombotic properties of this provisional pro-atherosclerotic ECM. J. Cell. Biochem. 101: 281,294, 2007. © 2007 Wiley-Liss, Inc. [source] PR-39 coordinates changes in vascular smooth muscle cell adhesive strength and locomotion by modulating cell surface heparan sulfate,matrix interactionsJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2001John H. Chon PR-39 is proline-rich peptide produced at sites of tissue injury. While the functional properties of this peptide have not been fully defined, PR-39 may be an important regulator of processes related to cell-matrix adhesion since it reportedly upregulates syndecan-4, which is a critical determinant of focal adhesion formation. The ability of PR-39 to modulate the adhesion and chemokinetic migration behavior of arterial smooth muscle cells (SMCs) in a fashion coordinated with syndecan-4 expression was investigated. Treatment of SMCs with PR-39 did not alter syndecan-1 mRNA, but did induce a two-fold increase in syndecan-4 mRNA (P,<,0.0001) and significantly enhanced cell surface expression of both syndecan-4 (P,<,0.01) and heparan sulfate (HS) (P,<,0.05). These observations were consistent with an observed increase in cell-matrix adhesive strength (P,<,0.05) and a reduction in cell speed (P,<,0.01) on fibronectin-coated substrates. Incubation of PR-39 treated cells with a soluble fibronectin derived heparin-binding peptide, as a competitive inhibitor of heparan sulfate/matrix interactions, abolished these effects. These data suggest that PR-39 mediated alterations of cell adhesion and motility may be related, in part, to the increased expression of heparan sulfate glycosaminoglycans (GAGs) that accompany the upregulation of cell surface syndecan-4. Futhermore, this investigation supports the notion that factors which control syndecan-4 expression may play an important role in regulating adhesion related cell processes. © 2001 Wiley-Liss, Inc. [source] 4-Aminopyridine affects rat arterial smooth muscle BKCa currents by changing intracellular pHBRITISH JOURNAL OF PHARMACOLOGY, Issue 8 2000Polina Petkova-Kirova The hypothesis whether or not 4-AP can affect vascular smooth muscle BKCa currents was tested using the patch-clamp technique, pH- and calcium-fluorimetry, and freshly isolated rat arterial smooth muscle cells. Application of 4-AP reversibly inhibited BKCa currents at an intracellular calcium ([Ca]i) of 250 nM with a half-block of 2.5 mM at +50 mV. The presence of 2 ,M thapsigargin, 10 ,M heparin, and 10 ,M ryanodine did not alter the effect of 4-AP on BKCa currents at [Ca]i 250 nM. At [Ca]i<100 nM 4-AP did not inhibit BKCa currents. Application of 4-AP to the intracellular or extracellular side of excised BKCa channels did not alter channel activity or channel amplitude. Replacement of the pH-sensitive calcium buffer EGTA by the pH-insensitive calcium buffer BAPTA in the intracellular solution turned the 4-AP-induced inhibition of BKCa currents into a stimulation at [Ca]i 250 nM. Application of 4-AP to single cells increased intracellular pH, which was accompanied by a reduction of [Ca]i in EGTA-loaded cells and a stable [Ca]i in BAPTA-loaded cells. Thus, these results suggest that in isolated vascular smooth muscle cells at [Ca]i>100 nM 4-AP affects BKCa currents via an alteration of intracellular pH. British Journal of Pharmacology (2000) 131, 1643,1650; doi:10.1038/sj.bjp.0703742 [source] Chlamydia pneumoniae and atherosclerosisCELLULAR MICROBIOLOGY, Issue 2 2004Robert J. Belland Summary Exposure to Chlamydia pneumoniae is extremely common, and respiratory infections occur repeatedly among most people. Strong associations exist between C. pneumoniae infection and atherosclerosis as demonstrated by: (i) sero-epidemiological studies showing that patients with cardiovascular disease have higher titres of anti- C. pneumoniae antibodies compared with control patients; (ii) detection of the organism within atherosclerotic lesions, but not in adjacent normal tissue by immunohistochemistry, polymerase chain reaction and electron microscopy and by culturing the organism from lesions; and (iii) showing that C. pneumoniae can either initiate lesion development or cause exacerbation of lesions in rabbit and mouse animal models respectively. The association of this organism with atherosclerosis has also provided sufficient impetus to conduct a variety of human secondary prevention antibiotic treatment trials. The results of these studies have been mixed and, thus far, no clear long-lasting benefit has emerged from these types of investigations. Studies of C. pneumoniae pathogenesis have shown that the organism can infect many cell types associated with both respiratory and cardiovascular sites, including lung epithelium and resident alveolar macrophages, circulating monocytes, arterial smooth muscle cells and vascular endothelium. Infected cells have been shown to exhibit characteristics associated with the development of cardiovascular disease (e.g. secretion of proinflammatory cytokines and procoagulants by infected endothelial cells and foam cell formation by infected macrophages). More detailed analysis of C. pneumoniae pathogenesis has been aided by the availability of genomic sequence information. Genomic and proteomic analyses of C. pneumoniae infections in relevant cell types will help to define the pathogenic potential of the organism in both respiratory and cardiovascular disease. [source] | ||||||||||