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Am J Physiol Heart Circ Physiol. 2000 Dec;279(6):H2829-37.
Mechanisms by which bradykinin promotes fibrosis in vascular smooth muscle cells: role of TGF-beta and MAPK.

Douillet CD, Velarde V, Christopher JT, Mayfield RK, Trojanowska ME, Jaffa AA.

Department of Medicine, Medical University of South Carolina, Charleston, USA.

Accumulation of extracellular matrix (ECM) is a hallmark feature of vascular disease. We have previously shown that hyperglycemia induces the expression of B(2)-kinin receptors in vascular smooth muscle cells (VSMC) and that bradykinin (BK) and hyperglycemia synergize to stimulate ECM production. The present study examined the cellular mechanisms through which BK contributes to VSMC fibrosis. VSMC treated with BK (10(-8) M) for 24 h significantly increased alpha(2)(I) collagen mRNA levels. In addition, BK produced a two- to threefold increase in alpha(2)(I) collagen promoter activity in VSMC transfected with a plasmid containing the alpha(2)(I) collagen promoter. Furthermore, treatment of VSMC with BK for 24 h produced a two- to threefold increase in the secretion rate of tissue inhibitor of metalloproteinase 1 (TIMP-1). The increase in alpha(2)(I) collagen mRNA levels and alpha(2)(I) collagen promoter activity, as well as TIMP-1 secretion, in response to BK were blocked by anti-transforming growth factor-beta (anti-TGF-beta) neutralizing antibodies. BK (10(-8) M) increased the endogenous production of TGF-beta1 mRNA and protein levels. Inhibition of the mitogen-activated protein kinase (MAPK) pathway by PD-98059 inhibited the increase of alpha(2)(I) collagen promoter activity, TIMP-1 production, and TGF-beta1 protein levels observed in response to BK. These findings provide the first evidence that BK induces collagen type I and TIMP-1 production via autocrine activation of TGF-beta1 and implicate MAPK pathway as a key player in VSMC fibrosis in response of BK.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11087238&dopt=Abstract

Am J Physiol Heart Circ Physiol. 2000 Dec;279(6):H2994-3002.
Effects of exercise training on cardiac function, gene expression, and apoptosis in rats.

Jin H, Yang R, Li W, Lu H, Ryan AM, Ogasawara AK, Van Peborgh J, Paoni NF.

Department of Cardiovascular Research, Genentech Incorporated, South San Francisco, California 94080, USA.

This study determined the effects of exercise training on cardiac function, gene expression, and apoptosis. Rats exposed to a regimen of treadmill exercise for 13 wk had a significant increase in cardiac index and stroke volume index and a concomitant decrease in systemic vascular resistance compared with both age-matched and body weight-matched sedentary controls in the conscious state at rest. In exercise-trained animals, there was no change in the expression of several marker genes known to be associated with pathological cardiac adaptation, including atrial natriuretic factor, beta-myosin heavy chain, alpha-skeletal and smooth muscle actins, and collagens I and III. Exercise training, however, produced a significant induction of alpha-myosin heavy chain, which was not observed in rats with myocardial infarction. No histological features of cardiac apoptosis were observed in the treadmill-trained rats. In contrast, apoptotic myocytes were detected in animals with myocardial infarction. In summary, exercise training improves cardiac function without evidence of cardiac apoptosis and produces a pattern of cardiac gene expression distinct from pathological cardiac adaptation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11087257&dopt=Abstract

Am J Physiol Heart Circ Physiol. 2000 Dec;279(6):H3031-9.
Urocortin, a member of the corticotropin-releasing factor family, in normal and diseased heart.

Nishikimi T, Miyata A, Horio T, Yoshihara F, Nagaya N, Takishita S, Yutani C, Matsuo H, Matsuoka H, Kangawa K.

Research Institute, National Cardiovascular Center, Suita, Osaka 565, Japan. nishikiokkyomed.ac.jp

In the present study we investigated the form of expression, action, second messenger, and the cellular location of urocortin, a member of the corticotropin-releasing factor (CRF) family, in the heart. Urocortin mRNA, as shown by quantitative RT-PCR analysis, is expressed in the cultured rat cardiac nonmyocytes (NMC) as well as myocytes (MC) in the heart, whereas CRF receptor type 2beta (CRF-R2beta), presumed urocortin receptor mRNA, is predominantly expressed in MC compared with NMC. Urocortin mRNA expression is higher in left ventricular (LV) hypertrophy than in normal LV, whereas CRF-R2beta mRNA expression is markedly depressed in LV hypertrophy compared with normal LV. Urocortin more potently increased the cAMP levels in both MC and NMC than did CRF, and its effect was more potent in MC than in NMC. Urocortin significantly increased protein synthesis by [(14)C]Phe incorporations and atrial natriuretic peptide secretion in MC and collagen and increased DNA synthesis by [(3)H]prolin and [(3)H]Thy incorporations in NMC. An immunohistochemical study revealed that urocortin immunoreactivity was observed in MC in the normal human heart and that it was more intense in the MC of the human failing heart than in MC of the normal heart. These results, together with the recent evidence of urocortin for positive inotropic action, suggest that increased urocortin in the diseased heart may modulate the pathophysiology of cardiac hypertrophy or failing heart, at least in part, via cAMP signaling pathway.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11087261&dopt=Abstract

Am J Physiol Heart Circ Physiol. 2000 Dec;279(6):H3124-30.
Design and construction of a uniaxial cell stretcher.

Yost MJ, Simpson D, Wrona K, Ridley S, Ploehn HJ, Borg TK, Terracio L.

Department of Developmental Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina 29208, USA. Yosed.sc.edu

In vitro mechanical cell stimulators are used for the study of the effect of mechanical stimulation on anchorage-dependent cells. We developed a new mechanical cell stimulator, which uses stepper motor technology and computer control to achieve a high degree of accuracy and repeatability. This device also uses high-performance plastic components that have been shown to be noncytotoxic, dimensionally stable, and resistant to chemical degradation from common culture laboratory chemicals. We show that treatment with glow discharge for 25 s at 20 mA is sufficient to modify the surface of the rubber to allow proper adhesion for polymerization of aligned collagen. We show through finite element analysis that the middle area of the membrane, away from the clamped ends, is predictable, homogeneous, and has negligible shear strain. To test the efficacy of the mechanical stretch, we examined the effect of mechanical stimulation on the production of beta(1)-integrin by neonatal rat cardiac fibroblasts. Mechanical stimulation was tested in the range of 0-12% stretch and 0-10-cycles/min stretch frequency. The fibroblasts respond with an increase in beta(1)-integrin at 3% stretch and a decrease at 6 and 12% stretch. Stretch frequency was found to not significantly effect the concentration of beta(1)-integrin. These studies yield a new and improved mechanical cell stimulator and demonstrate that mechanical stimulation has an effect on the expression of beta(1)-integrin.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11087271&dopt=Abstract

J Invest Dermatol. 2003 Jan;120(1):153-63.
Severely impaired wound healing in the collagenase-resistant mouse.

Beare AH, O'Kane S, Krane SM, Ferguson MW.

Division of Immunology, Microbiology and Development, and UK Centre for Tissue Engineering, School of Biological Sciences, University of Manchester, UK.

Collagen in the skin undergoes dramatic reorganization during wound repair. Matrix metalloproteinases degrade and remodel the collagen in a tightly controlled process. The collagenase-resistant mouse, Col1a1(tm1Jae), has been developed to produce collagen type I, which is resistant to degradation by human matrix metalloproteinase 1. These mice grow normally but develop thickened skin with age. We investigated the effect of this mutant collagen on wound repair. Incisional wounds were made on Col1a1(tm1Jae) homozygous mutant (Col1a1(r/r)) and wild-type (Col1a1+/+) mice and these wounds were harvested at 1 and 6 h, 1, 2, 3, 7, 10, 14, and 70 d post wounding. Wound healing was severely delayed in Col1a1(r/r) wounds, with wounds remaining significantly wider than wild-type for the first 2 wk after injury. Reepithelialization of the Col1a1(r/r) wounds took 7 d longer than in the wild-type. The Col1a1(r/r) wounds had a prolonged early inflammatory response. Immunostaining for matrix metalloproteinases revealed significant upregulation of matrix metalloproteinase 13 in Col1a1(r/r) wounds, but minimal changes in other matrix metalloproteinases. There was no significant difference in scarring between Col1a1(r/r) and Col1a1+/+ wounds after 70 d.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535212&dopt=Abstract

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