PDGF-beta receptor and PKC have no effect on angiotensin II-induced JAK2 and STAT1 phosphorylation in vascular smooth muscle cells under high glucose condition

Ozturk O. H., ÇETİN A., Tokay A., Uzuner F., TANRIÖVER G., YEŞİLKAYA A.

JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION, cilt.31, sa.5, ss.340-349, 2011 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 31 Sayı: 5
  • Basım Tarihi: 2011
  • Doi Numarası: 10.3109/10799893.2011.592535
  • Dergi Adı: JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.340-349
  • Anahtar Kelimeler: JAK-STAT, angiotensin II, high glucose, PKC, PDGF-beta receptor, PROTEIN-KINASE-C, GROWTH-FACTOR-BETA, JAK/STAT PATHWAY, SIGNAL-TRANSDUCTION, INDUCED ACTIVATION, DIABETES-MELLITUS, OXIDATIVE STRESS, TYROSINE KINASE, MESANGIAL CELLS, TRANSACTIVATION
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Background: The mechanisms responsible for the accelerated cardiovascular disease in diabetes, as well as the increased hypertrophic effects of angiotensin II (Ang II) under hyperglycemic condition, are not very clear. Evidences show that platelet-derived growth factor (PDGF) and protein kinase C (PKC) play a critical role in this effect. In our study, we examined the role of PKC and PDGF receptor on JAK2 and STAT1 phosphorylation under high glucose (HG) condition (25 mmol/L) in response to Ang II in cultured vascular smooth muscle cells (VSMC).