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Titolo:
REGULATION OF VASCULAR CONNEXIN43 GENE-EXPRESSION BY MECHANICAL LOADS
Autore:
COWAN DB; LYE SJ; LANGILLE BL;
Indirizzi:
TORONTO HOSP,GEN DIV,RES INST,CCRW 1-836,200 ELIZABETH ST TORONTO ON M5G 2C4 CANADA TORONTO HOSP,GEN DIV,RES INST TORONTO ON M5G 2C4 CANADA MT SINAI HOSP,SAMUEL LUNENFELD RES INST TORONTO ON M5G 1X5 CANADA UNIV TORONTO,DEPT LAB MED & PATHOBIOL TORONTO ON CANADA UNIV TORONTO,DEPT PHYSIOL TORONTO ON CANADA UNIV TORONTO,DEPT OBSTET & GYNECOL TORONTO ON CANADA
Titolo Testata:
Circulation research
fascicolo: 7, volume: 82, anno: 1998,
pagine: 786 - 793
SICI:
0009-7330(1998)82:7<786:ROVCGB>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAP JUNCTION PROTEIN; SMOOTH-MUSCLE CELLS; FLUID SHEAR-STRESS; GLUTATHIONE-PEROXIDASE GENE; FACTOR-B-CHAIN; ENDOTHELIAL-CELL; GROWTH-FACTOR; IN-VIVO; PROTOONCOGENE EXPRESSION; MAMMALIAN-CELLS;
Keywords:
VASCULAR REMODELING; GAP JUNCTION; CELL STRETCH; SHEAR STRESS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
66
Recensione:
Indirizzi per estratti:
Citazione:
D.B. Cowan et al., "REGULATION OF VASCULAR CONNEXIN43 GENE-EXPRESSION BY MECHANICAL LOADS", Circulation research, 82(7), 1998, pp. 786-793

Abstract

Vascular tissues respond to changes in the mechanical forces imposed on them with changes in vasomotor tone in the short term and with structural remodeling in the long term. Since these responses involve intercellular communication, we have investigated regulation of the gap junction proteins, connexin26 (Cx26), connexin37 (Cx37), connexin40 (Cx40), and connexin43 (Cx43), by mechanical loads. Results were compared with parallel experiments on c-fos and GAPDH. Twenty percent stretch of cultured vascular smooth muscle cells caused a 3-fold increase in Cx43 mRNA levels by 2 hours. Cx26 was expressed at low levels but failedto respond to stretch, and Cx37 and Cx40 were not detected. c-Sos mRNA levels increased after 30 minutes of stretch, whereas GAPDH mRNA didnot change. Protein levels of Cx43 increased by 4 hours and remained elevated for 16 hours. Nuclear run-on experiments confirmed that Cx43 and c-fos were transcriptionally regulated by stretch, New protein synthesis was not a requirement for the stretch-induced rise in Cx43 expression, since mRNA levels were unaffected by treatment with cycloheximide, To examine transcriptional control of Cx43, stretched and unstretched vascular smooth muscle cells were transfected with a variety of promoter-reporter gene constructs. Cx43 sequences extending from withinexon 1 (+162) to -1686 in the 5'-flanking region were coupled to the chloramphenicol acetyl transferase reporter gene. Deletions from the 5' end of these sequences differentially regulated reporter gene expression and indicated multiple potential regulatory sites. in particular,a putative activator protein-1 site at the -42 to -48 region was required for basal reporter activity. None of the promoter constructs revealed stretch sensitivity, indicating that the site of transcriptional control by stretch lies outside the -1686 to +162 region, Finally, Cx43 mRNA levels were assessed in cultured endothelial cells subjected tolaminar shear stress of 15 dynes/cm(2). Cx43 mRNA levels increased byapproximate to 4-fold at 1 hour and remained elevated for the duration of shear force. In conclusion, both mechanical strain and fluid sheer stress caused increased expression of the gap junction protein Cx43.

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Documento generato il 28/09/20 alle ore 05:02:50