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Many researches showed that stress induced the cardiovascular disease, which happened basis on the cardiomyocytes apoptosis.Recent investigation indicates that treated with apoptosis inducers, NGFI-B translocate from nucleus to cytoplasm.The role of NGFI-B and its molecular basis under stress, however, is not clear.Our investigation indicates that NGFI-B translocate from nucleus to mitochondria in stress incuced cardiomyocytes apoptosis.The study was designed to determine the role of NGFI-B in cardiomyocytes of restraint-stressed rats.Co-immunonoprecipitation shown that GRP75 is bound to NGFI-B in mitochondria of stressed cardiomyocytes.But they were not finding to bind together in mitochondria of unstressed cardiomyocytes.Overexpression of GRP75 could inhibit the activition of apoptosis pathway induced by NGFI-B.Suggested that promotion apoptosis of NGFI-B was implemented through GRP75.Overexpression of NGFI-B induced the disorder of MPTP and energy metabolism.GRP75 protected against the disorder of MPTP and energy metabolism induced by over expression of NGFI-B under stress.Indicated that NGFI-B induced apoptosis by mediates the disorder of MPTP and energy metabolism through GRP75.Thus, GRP75 in mitochondria is the key target point, by which NGFI-B mediates cardiomyocytes apoptosis.