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Basic science: Cardiovascular disease basic research
e0159 Osteopontin is involved in urotensin II induced migration of adventitial fibroblasts from rat aorta
  1. Zhang Yonggang1,
  2. Kuang Zejian1,
  3. Mao Yanyan1,
  4. Wei Ruihong2,
  5. Bao Shilin1,
  6. Wu Libiao1,
  7. Hu Yanchao1
  1. 1First Affiliated Hospital, Shantou University Medical College, Shantou, China
  2. 2Second Affiliated Hospital, Shantou University Medical College, Shantou, China

Abstract

Background Recent studies suggest osteopontin (OPN) plays a critical role in the progression of vascular remodelling, and that Urotensin II (UII) is a potent vasoconstrictor and stimulator of cellular migration. The goal of this study was to test the hypothesis that OPN is involved in UII-induced migration of rat aortic adventitial fibroblasts (AFs), and examine the effect and mechanisms of UII on OPN expression.

Design Growth-arrested AFs were incubated in serum-free medium with UII and some inhibitors of signal transduction pathways. Cell migration was determined by a transwell technique. The OPN mRNA expression and protein secretion induced by UII were evaluated by the reverse transcriptase PCR and ELISA method, respectively.

Results OPN antisense oligonucleotides inhibited UII-induced AFs migration significantly compared with UII (10−8 mol/l) group (p<0.05). Moreover, UII promoted the OPN mRNA expression and protein secretion in a dose-dependent and time-dependent manner, with maximal effect at a concentration of 10−8 mol/l at 3 h for mRNA expression, or at 24 h for protein secretion, respectively (p<0.01). The UII receptor antagonist SB710411 (10−6mol/l), Ca2+ channel blocker nicardipine (10−5 mol/l), protein kinase C inhibitor H7 (10−5 mol/l), calcineurin inhibitor cyclosporine A (10−5 mol/l), Rho kinase inhibitor Y-27632 (10−5 mol/l) and mitogen activated protein kinase (MAPK) inhibitor PD98059 (10−5 mol/l) inhibited the UII effects significantly.

Conclusion This study indicated that UII may up-regulate OPN expression in AFs through the UII receptor, protein kinase C, MAPK, calcineurin, Rho kinase and Ca2+ signal transduction pathways, and OPN is involved in UII-induced AFs migration.

  • Urotensin II
  • osteopontin
  • adventitial fibroblasts
  • migration
  • vascular remodelling

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