Key result
Hypertensive rats with diastolic heart failure exhibit enhanced cardiomyocyte GRP78 and caspase-12 expression.
Why the study?
The expression of GRP78 and caspase-12 in diastolic heart failure resulting from hypertension remains poorly understood.
Hypothesis-generating in hypertensive rat model; leaves open human relevance and therapeutic potential.
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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Sun et al. (2008) studied Diastolic heart failure resulting from hypertension. Diastolic heart failure resulting from hypertension was evaluated on Expression of GRP78 and caspase-12 at protein and mRNA levels. GRP78 and caspase-12 had enhanced expression at protein and mRNA levels in cardiomyocytes of spontaneously hypertensive rats with diastolic heart failure.