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Upregulation of GRP78 and caspase-12 in diastolic failing heart

100%

Sun Y., Liu G., Song T., Liu F., Kang W., Zhang Y., Ge Z.

Acta Biochimica Polonica

2008

tom 55

nr 3

511-516

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.

Co-involvement of the mitochondria and endoplasmic reticulum in cell death induced by the novel ertargeted protein HAP

67%

Xu H., Zhou Q., Liu X., Qi Y.

Cellular and Molecular Biology Letters

2006

tom 11

nr 2

HAP (a homologue of the ASY/Nogo-B protein), a novel human apoptosis-inducing protein, was found to be identical to RTN3. In an earlier study, we demonstrated that HAP localized exclusively to the endoplasmic reticulum (ER) and that its overexpression could induce cell apoptosis via a depletion of endoplasmic reticulum (ER) Ca2+ stores. In this study, we show that overexpression of HAP causes the activation of caspase-12 and caspase-3. We still detected the collapse of mitochondrial membrane potential (Δωm) and the release of cytochrome c in HAP-overexpressing HeLa cells. All the results indicate that both the mitochondria and the ER are involved in apoptosis caused by HAP overexpression, and suggest that HAP overexpression may initiate an ER overload response (EOR) and bring about the downstream apoptotic events.

Ograniczanie wyników

1 Acta Biochimica Polonica

1 Cellular and Molecular Biology Letters

1 Ge Z.

1 Kang W.

1 Liu F.

1 Liu G.

1 Liu X.

1 Qi Y.

1 Song T.

1 Sun Y.

1 Xu H.

1 Zhang Y.

1 Zhou Q.

1 2008

1 2006

Wyniki wyszukiwania

Upregulation of GRP78 and caspase-12 in diastolic failing heart

Co-involvement of the mitochondria and endoplasmic reticulum in cell death induced by the novel ertargeted protein HAP