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Titolo:
Protein kinase C activation contributes to microvascular barrier dysfunction in the heart at early stages of diabetes
Autore:
Yuan, SY; Ustinova, EE; Wu, MH; Tinsley, JH; Xu, WJ; Korompai, FL; Taulman, AC;
Indirizzi:
Texas A&M Univ, Syst Hlth Sci Ctr, Cardiovasc Res Inst, Dept Surg, Temple,TX 76504 USA Texas A&M Univ Temple TX USA 76504 s Inst, Dept Surg, Temple,TX 76504 USA Texas A&M Univ, Syst Hlth Sci Ctr, Cardiovasc Res Inst, Dept Med Physiol, Temple, TX 76504 USA Texas A&M Univ Temple TX USA 76504 Dept Med Physiol, Temple, TX 76504 USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 5, volume: 87, anno: 2000,
pagine: 412 - 417
SICI:
0009-7330(20000901)87:5<412:PKCACT>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
CAPILLARY-PERMEABILITY; ENDOTHELIAL-CELLS; CORONARY VENULES; GLUCOSE-LEVELS; ALBUMIN; RATS; COMPLICATIONS; INHIBITOR; MELLITUS; PERMEATION;
Keywords:
diabetes; microcirculation; permeability; protein kinases;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Yuan, SY Texas A&M Univ, Syst Hlth Sci Ctr, Cardiovasc Res Inst, Dept Surg, 1901 S 1st St,Bldg 4, Temple, TX 76504 USA Texas A&M Univ 1901 S 1st St,Bldg 4 Temple TX USA 76504 76504 USA
Citazione:
S.Y. Yuan et al., "Protein kinase C activation contributes to microvascular barrier dysfunction in the heart at early stages of diabetes", CIRCUL RES, 87(5), 2000, pp. 412-417

Abstract

The functional disturbance of microvasculature is recognized as an initiating mechanism that underlies the development of various diabetic complications. Although a causal relationship between microvascular leakage and tissue damage has been well documented in diabetic kidneys and eyes, there is a lack of information regarding the barrier function of coronary exchange vessels in the disease state. The aim of the present study was to evaluate thepermeability property of coronary microvessels during the early development of experimental diabetes with a focus on the protein kinase C (PKC)-dependent signaling mechanism. The apparent permeability coefficient of albumin (Pa) was measured in isolated and perfused porcine coronary venules. The administration of high concentrations of D-glucose induced a dose-dependent increase in the Pa value, which was prevented by blockage of PKC with its selective inhibitors bisindolylmaleimide and Goe 6976. More importantly, an elevated basal permeability to albumin was observed in coronary venules at the early onset of streptozotocin-induced diabetes. The hyperpermeability was corrected with bisindolylmaleimide and the selective PKC beta inhibitor hispidin. Concomitantly, protein kinase assay showed a high PKC activity in isolated diabetic venules. Immunoblot analysis of the diabetic heart revealed a significant subcellular translocation of PKC beta II and PKC epsilon from the cytosol to the membrane, indicating that the specific activity of these isoforms was preferentially elevated. The results suggest that endothelial barrier dysfunction attributed to the activation of PKC occurs at the coronary exchange vessels in early diabetes.

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Documento generato il 07/07/20 alle ore 12:44:29