Basic & Clinical Medicine ›› 2012, Vol. 32 ›› Issue (3): 305-308.

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Activation of ERK Pathway by EGF and Angiotensin II in Adrenocortical Carcinoma H295R Cells

TONG An-li   

  • Received:2011-12-22 Revised:2012-01-11 Online:2012-03-05 Published:2012-02-27
  • Contact: TONG An-li E-mail:tonganli@hotmail.com

Abstract: Objectives: To study the effects of EGF and angiotensinII on ERK pathways in adrenocortical carcinoma H295R Cells. Methods: Treated with EGF and angiotensin II with different concentrations, phosphorylation of ERK1/2 was detected by Western blot. The effect of Angiotensin II on phospho-ERK1/2 was also observed when pretreated with the specific inhibitor of the EGF receptor tyrosine kinase, AG1478. Treated with EGF and angiotensin II alone or both, phosphorylation of ERK1/2,p90RSK and Bad was detected. Results: Both EGF and angiotensin II increased phospho-ERK1/2 in a dose-dependent manner, and they also promoted phospho-p90RSK. EGF and angiotensin II showed an additive effect on phosphorylation of ERK1/2 and p90RSK. Treated by Angiotensin II and EGF alone or both, phospho-ERK1/2 were 6.3±1.4、2.2±0.6 and 10.1±1.1, respectively, relatived to the control. Angiotensin II, but not EGF, stimulated phospho-Bad. The effects of angiotensin II on phospho-ERK1/2 was not blocked by AG1478. Conclusion: Both EGF and Angiotensin II promotes ERK pathway, and they show an additive effect in H295R cells.

Key words: EGF, H295R cell, pathway, angiotensin II

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