title: Upregulation of GRP78 and caspase-12 in diastolic failing heart.
abstract: BACKGROUND
  The endoplasmic reticulum (ER) fulfills multiple cellular functions. Various stimuli can potentially cause ER stress (ERS). ERS is one of the intrinsic apoptosis pathways and apoptosis plays a critical role in hypertension. Glucose regulated protein 78 (GRP78) has been widely used as a marker for ERS and caspase-12 mediated apoptosis was a specific apoptotic pathway of ER. The expression of GRP78 and caspase-12 remains poorly understood in the diastolic heart failure resulting from hypertension.
  
  
  METHODS
  We used spontaneously hypertensive rats (SHRs) to establish a model of diastolic heart failure, and performed immunohistochemistry, western blot, and real-time PCR to analyze GRP78 and caspase-12.
  
  
  RESULTS
  We found that GRP78 and caspase-12 had enhanced expression at protein and mRNA levels.
  
  
  CONCLUSIONS
  These results suggest that GRP78 and caspase-12 were upregulated in cardiomyocytes and ERS can contribute to cardiac myocyte apoptosis in the diastolic heart failure resulting from hypertension.
authors.affiliation: Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiovascular Disease, Qilu Hospital, Shandong University, Jinan, China.
authors.forename: Yingying
authors.initials: Y
authors.lastname: Sun
authors.forename: Guanghui
authors.initials: G
authors.lastname: Liu
authors.forename: Tao
authors.initials: T
authors.lastname: Song
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.forename: Weiqiang
authors.initials: W
authors.lastname: Kang
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zhiming
authors.initials: Z
authors.lastname: Ge
mesh_terms: D000818:Animals; D017209:Apoptosis; D001483:Base Sequence; D053454:Caspase 12 / Q000235:genetics* / Q000378:metabolism*; D017931:DNA Primers / Q000235:genetics; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000378:metabolism; D054144:Heart Failure, Diastolic / Q000209:etiology / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D006360:Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism*; D006973:Hypertension / Q000150:complications; D008297:Male; D018832:Molecular Chaperones / Q000235:genetics* / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013312:Stress, Physiological; D015854:Up-Regulation; D000091342:Endoplasmic Reticulum Chaperone BiP
chemical_list: D053454:Caspase 12; D017931:DNA Primers; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D012333:RNA, Messenger; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP; C506443:Casp12 protein, rat