Abstract
Early growth response, Egr‐1, is known to activate the expression of several genes implicated in the development of vascular dysfunction. Earlier studies have shown that angiotensin II (AngII) enhances the expression of Egr‐1 and Giα proteins in vascular smooth muscle cells (VSMC). In addition, the role of enhanced levels of endogenous Ang II in enhanced expression of Giα proteins in spontaneously hypertensive rats (SHR) has also been shown. The present study was therefore undertaken to examine if VSMC from SHR also exhibit enhanced expression of Egr‐1 proteins and explore the underlying molecular mechanisms mediating this effect. The levels of Egr‐1 protein in VSMC from SHR were not different in 2 weeks old SHR as compared to WKY (Wistar‐Kyoto rats), however, it started increasing at 4 weeks and at 12 weeks, it was significantly increased by 80%. Knockdown of Giα‐2 proteins, using antisense and siRNA treatment, attenuated the enhanced expression of Egr‐1 proteins to control levels. In addition, the knockdown of Egr‐1 by siRNA also attenuated the expression of Giα‐2 and Giα‐3 proteins in VSMC from 12 week old SHR. The enhanced levels of Egr‐1 protein were attenuated by losartan (an AT1 receptor antagonist), BQ123 (an ETA receptor antagonist), BQ788 (an ETB receptor antagonist) but not by PD123319 (an AT2 receptor antagonist) in VSMC from 12 week SHR. These results suggest that VSMC from SHR exhibit an overexpression of Egr‐1 which is due to the enhanced levels of endogenous Ang II, ET‐1 and Giα proteins. In addition, Egr‐1 also regulates the expression of Giα proteins in VSMC from SHR and suggests a cross‐talk between Giα and Egr‐1.Support or Funding InformationSupported by CIHRThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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