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

Basit Öğe Kaydı
dc.authoridTOKAY, ALPER/0000-0002-2394-5555
dc.contributor.authorOzturk, Oktay Hasan
dc.contributor.authorCetin, Arzu
dc.contributor.authorTokay, Alper
dc.contributor.authorUzuner, Fatih
dc.contributor.authorTanriover, Gamze
dc.contributor.authorYesilkaya, Akin
dc.date.accessioned2024-09-18T20:28:11Z
dc.date.available2024-09-18T20:28:11Z
dc.date.issued2011
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBackground: 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). Methods: VSMCs were isolated from the thoracic aorta of male Wistar rats and were cultured. Growth-arrested VSMCs were placed in either normal glucose (NG) or HG condition for 48 h and then VSMCs were stimulated with agonists and antagonists. The tyrosine phosphorylation of JAK2 or STAT were determined by immunoblotting using specific antibodies. Results: High glucose markedly increased the phosphorylation of tyrosine residues of JAK2 and serine residues of STAT 1 compared with cells cultured in NG (5.5 mmol/L) with and without Ang II stimulation. Experiments made with specific PDGF-beta receptor inhibitor AG1295 and PKC inhibitor GF109203X showed that there were no changes in Ang II-stimulated JAK2 and STAT1 phosphorylation under NG and HG conditions compared with experiments without inhibitors. Conclusion: According to our findings, Ang II-stimulated JAK2 and STAT1 phosphorylation under either NG or HG condition do not proceed via a different pathway rather than PKC and PDGF-beta receptor.en_US
dc.description.sponsorshipAkdeniz University Scientific Research [2003.03.0122.002]en_US
dc.description.sponsorshipThis study was supported by Akdeniz University Scientific Research Projects Fund with Project No: 2003.03.0122.002.en_US
dc.identifier.doi10.3109/10799893.2011.592535
dc.identifier.endpage349en_US
dc.identifier.issn1079-9893
dc.identifier.issn1532-4281
dc.identifier.issue5en_US
dc.identifier.pmid21929289en_US
dc.identifier.scopus2-s2.0-80053000945en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage340en_US
dc.identifier.urihttps://doi.org/10.3109/10799893.2011.592535
dc.identifier.urihttps://hdl.handle.net/20.500.12483/10783
dc.identifier.volume31en_US
dc.identifier.wosWOS:000295002700003en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofJournal of Receptors and Signal Transductionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectJAK-STATen_US
dc.subjectangiotensin IIen_US
dc.subjecthigh glucoseen_US
dc.subjectPKCen_US
dc.subjectPDGF-beta receptoren_US
dc.titlePDGF-? receptor and PKC have no effect on angiotensin II-induced JAK2 and STAT1 phosphorylation in vascular smooth muscle cells under high glucose conditionen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
[ N/A ]
İsim:
Tam Metin / Full Text
Boyut:
1.14 MB
Biçim:
Adobe Portable Document Format
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu