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• W611136307 abstract "Understanding the mechanisms that underly smooth muscle hypertrophy is a major issue in vascular pathology. In fact increase in vascular smooth muscle cell (VSMC) size is frequently associated with hypertension, not only as resulting from mechanical overload but also as a causative factor for vessel remodelling leading to elevated blood pressure. Our experimental model are peritubular smooth muscle cells (PSMC) from rat testis. They are an epithelioid contractile layer surrounding the seminiferous epithelium and are responsible for the propulsion of sperm along seminiferous tubules. PSMC lack the SMC characteristic elongated shape but show specific smooth muscle markers like -sm-actin, sm-myosin, desmin and ETA and ETB endothelin receptors. At variance with other types of smooth muscle cells, PSMC can be cultured in simple serum-free medium under totally controlled conditions maintaining traits of the contractile phenotype, such as the expression of specific isoactin and responsiveness to the potent conctractile agonist endothelin-1 (ET-1).The present study investigates the long term hypertrophic response and the transduction pathways involved in up-regulation of the differentiated phenotype and induction of hypertrophy in PSMC by PDGF-BB and ET-1. Cell hypertrophy is a well known response of muscle cells to long term stimulation with agonists of contraction. This reactive behaviour, characterised by an increase in cell size and myofilament components as well as by increased protein synthesis, is known to take place not only in striated muscle but also in smooth muscle cells. On the other hand, a comprehensive model of how smooth muscle cell hypertrophy develops is so far lacking. At variance with striated muscle, smooth muscle differentiated phenotype is labile, both in vitro and in vivo. In these conditions of plasticity, the identification of the specific intracellular pathways responsible for the maintenance of the smooth muscle contractile phenotype and for the development of cell hypertrophy has so far proved elusive. In PSMC the growth factor PDGF-BB unespectedly fails to induce proliferation but rather induces transitory cell contraction followed by cell hypertrophy. In order to extend our previous data on the role of MAPK in PSMC cell hypertrophy, the possible role of p38 has been investigated. This MAPK is rapidly activated by PDGF-BB and when stimulated in the presence of the p38 inhibitor SB203580 cells were found to contain about half -SM actin and failed to develop sm--actin-containing stress fibers; cytofluorimetric analysis of cell size showed that SB203580 significantly and dose dependently reduced the hypertrophic response. Comparable results, decrease of sm--actin syntesis, no formation of sm--actin stress fibers and block of cellular size increase, were observed when the response to PDGF-BB was studied in the continuous presence of Y27632, an inhibitor of the Rho-dependent kinase ROCK. The transcription factor nucleosomal kinase MSK1, downstream target of p38, was activated by PDGF-BB, and p38 inhibitor SB203580 inhibited its phosphorylation which appeared unaffected by ROCK inhibitor Y27632. In concluding, p38 and the Rho-ROCK system were found to play a prominent, likely independent, role in the up-regulation of PSMC differentiated phenotype and induction of hypertrophy by PDGF-BB.As for ET-1, long term treatment of PSMC with this agonist of contraction did not induce proliferation, but was found to stimulate general protein syntesis. Moreover, treatment of PSMC with IRL1620, specific agonist of ETB receptor, or with ET-1 plus BQ788, specific inhibitor of ETB, shows that both receptors are implicated in the long term response to ET-1. In all cases we assist to the increase of specific contractile markers syntesis: sm--actin, desmin, caldesmon and calponin. In particular stimulation of ET-1 receptors, in combination or separately, results in the formation of sm--actin stress fibers and in increase of desmin intermediate filaments. The potentiation of the differentiated phenotype is accompanied by an increase of cell size evaluated by cytofluorimetric analysis. In concluding, the hypertrophic phenotype induced by long term treatment with ET-1 is mediated by the two receptors independently. Moreover, molecular analysis shows that the role of PKC is not important to the induction of PSMC hypetrophy, but the pathway RhoA-ROCK may have a role in the potentiation of contractile phenotype through ETB receptor." @default.
• W611136307 created "2016-06-24" @default.
• W611136307 creator A5042467690 @default.
• W611136307 date "2006-03-06" @default.
• W611136307 modified "2023-09-26" @default.
• W611136307 title "Regolazione del fenomeno contrattile nelle cellule muscolari lisce" @default.
• W611136307 hasPublicationYear "2006" @default.
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