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INHIBITS ANGIOTENSIN II-INDUCED CELL GROWTH VIA SHIP2 AND 4E-BP1
1 Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: ernesto.schiffrin{at}ircm.qc.ca.
Objective: The present study evaluated the effects of peroxisome proliferator-activated receptor (PPAR)-
activators on angiotensin (Ang) II-induced signaling pathways and cell growth.
Methods and Results: Vascular smooth muscle cells (VSMC) derived from rat mesenteric arteries were treated with Ang II, with/without the AT1 recptor blocker valsartan or the AT2 receptor blocker PD123319, after pre-treatment for 24h with the PPAR- activators 15-deoxy-
12,14-prostaglandin J2 (15d-PGJ2) or rosiglitazone. Both 15d-PGJ2 and rosiglitazone decreased Ang II-induced DNA synthesis. Rosiglitazone treatment increased nuclear PPAR- expression and activity in VSMC. However, rosiglitazone did not alter expression of PPAR-
/
, ERK1/2, Akt or Ang II receptors. 15d-PGJ2 and rosiglitazone decreased ERK1/2 and Akt peak activity, both of which were induced by Ang II via the AT1 the receptor. Rosiglitazone inhibited Ang II enhanced phosphorylation of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), as well as Src homology 2-containing inositol phosphatase 2 (SHIP2). Conclusions: PPAR- activation reduced Ang II-induced growth associated with inhibition of ERK1/2, Akt, 4E-BP1 and SHIP2. Modulation of these pathways by PPAR- activators may contribute to regression of vascular remodeling in hypertension.
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