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Upregulation of GRP78 and caspase-12 in diastolic failing heart.

Authors: Sun, Y  Liu, G  Song, T  Liu, F  Kang, W  Zhang, Y  Ge, Z 
Citation: Sun Y, etal., Acta Biochim Pol. 2008;55(3):511-6. Epub 2008 Sep 12.
Pubmed: (View Article at PubMed) PMID:18787714

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.

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RGD Object Information
RGD ID: 2311453
Created: 2009-07-17
Species: All species
Last Modified: 2009-07-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.