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. Author manuscript; available in PMC: 2014 Oct 9.
Published in final edited form as: Int J Cardiol. 2013 May 3;168(4):3291–3299. doi: 10.1016/j.ijcard.2013.04.045

Figure 8.

Figure 8

Upregulation of PCMT1 attenuates Mst1 activation and cell apoptosis under hypoxic conditions. A, NRCMs were treated with either vehicle or CGP3466P as indicated for twelve hours. Total RNA was extracted and then subjected to the analysis for the expression of PCMT1 by qRT-PCR. B, Cardiomyoctes were treated with either vehicle or CGP3466P for twenty-four hours. Extracted cell lysates were subjected to the analysis of the expression of PCMT1 by Western blot. C, NRCMs were pretreated with either vehicle or CGP3466P for twenty-four hours and then subjected to hypoxia/reoxygenation. Mst1 was then immunoprecipitated and its activity was determined by an in vitro kinase assay using histone H2B as a substrate. N indicates normoxia; HR, hypoxia/reoxygenation. D, Forty-eight hours after transfection with either control siRNA or PCMT1 siRNA, NRCMs were treated with either vehicle or CGP3466B for twenty-four hours and then subjected to hypoxia/reoxygenation injury as indicated. Cell apoptosis was quantitated by In Situ Cell Death Detection kit (Roche). The data are representatives of 4 independent experiments.