mHGTD-P mediates hypoxic neuronal cell death via the release of apoptosis-inducing factor

Cho, Young-Eun; Ko, Jeong‐Hun; Kim, Yong-Jun; Yim, Ji-Hye; Kim, Su-Mi; Park, Jaehoon

doi:10.1016/j.neulet.2007.01.073

Cited by 9 publications

(11 citation statements)

References 22 publications

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“…8 Previous studies showed that HGTD-P exerted proapoptotic effects in a cell typespecific manner. 8,9 In the present study, we reported for the first time on the role and mechanism of HGTD-P in regulating neuronal apoptosis in developing rat brain with HI.…”

Section: Discussionmentioning

confidence: 61%

“…These findings differ from those obtained in mouse neurons, in which the proapoptotic effect of HGTD-P was found to depend only on AIF translocation and not on activation of caspases. 9 This discrepancy may result from the difference in cell types in the 2 studies, or from the difference of the extent and duration of HI. How HGTD-P regulates neuronal apoptosis remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…8 In contrast, studies on mouse neuronal cultures indicate that HGTD-P induces cell apoptosis by promoting the translocation of apoptosisinducing factor (AIF) from mitochondria to the nucleus, independent of cytochrome C release and caspase activation. 9 Collectively, these findings suggest that HGTD-P may function differently in regulating apoptosis in different types of cells or animals.…”

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confidence: 97%

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Proapoptotic Role of Human Growth and Transformation-Dependent Protein in the Developing Rat Brain After Hypoxia-Ischemia

Mao

Zhao

et al. 2009

Stroke

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Background and Purpose-Human growth and transformation-dependent protein (HGTD-P) is a new proapoptotic protein and an effector of cell death induced by hypoxia-ischemia (HI). The function of HGTD-P has been investigated in human prostate cancer cells and mouse neurons cultured in vitro. However, whether HGTD-P is involved in regulating the apoptosis of rat neurons is not clear, and the relevance of HGTD-P in HI animal models is still unknown. Therefore, in the present study, we tried to elucidate the role that HGTD-P plays in apoptosis of rat neurons subjected to HI, both in culture and in the developing rat brain in vivo. Methods-Samples from primary cultured neurons and postnatal day 10 rat brains with HI were collected. RT-PCR, Western blotting, and immunocytochemistry were used to detect the expression and distribution of rat HGTD-P, cleaved caspase 3, and apoptosis-inducing factor (AIF). MTT assay, DAPI, TUNEL, and flowcytometry were used to detect cell viability and apoptosis. Results-We found that HI upregulated the mRNA and protein levels of HGTD-P in rat neurons in vitro and in vivo.Antisense oligonucleotides (AS) targeted to HGTD-P inhibited the expression of HGTD-P, thus rescuing neuronal viability and attenuating neuronal apoptosis. In addition, we found that HGTD-P played its proapoptotic role by activating caspase 3 and inducing the translocation of AIF to nuclear. Conclusions-Our findings show that HGTD-P plays a proapoptotic role in the developing rat brain after HI and that it may be a potential target in treating HI-induced brain damage.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

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Proapoptotic Role of Human Growth and Transformation-Dependent Protein in the Developing Rat Brain After Hypoxia-Ischemia

Mao

Zhao

et al. 2009

Stroke

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“…Diverse pathways are involved in hypoxic neuronal cell death [20] . For example, ischemic injury to the brain induces necrosis of neurons at the core of the lesion but triggers caspase-sensitive apoptotic cell death at the periphery [21] .…”

Section: Discussionmentioning

confidence: 99%

Caspase-9-Dependent Nuclear Translocation of Cytochrome <i>c</i> in Hypoxic Injury

Kim¹,

Kim²,

Seok³

et al. 2010

Pathobiology

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Objective: Hypoxia signals the release of cytochrome c from mitochondria as well as sequential activation of caspase-9 and caspase-3 in the pathway to apoptosis. In this report, we describe novel mechanisms governing the nuclear translocation of cytochrome c during hypoxia-induced apoptosis in neuroepithelioma, SK-N-MC cells. Methods: This work focuses on an investigation of the mechanism of cytochrome c translocation by means of immunocytochemistry, cell fractionation, Western blot and caspase assay. Results: Using immunocytochemistry and subcellular fractionation, we found that caspase-9 activation precedes cytochrome c release and translocation. Inhibition of caspase-9 activity blocked these responses to hypoxia. Previous studies suggest a key role for c-Jun N-terminal kinase (JNK) in apoptosis regulation and accordingly we found that JNK activation was essential for caspase-9 activation and nuclear translocation of cytochrome c. Conclusions: In this report, we describe novel mechanisms of caspase-9-dependent nuclear translocation of cytochrome c in hypoxic injury.

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“…HGTD-P-overexpressing cells undergo apoptotic cell death in a caspase-dependent or caspase-independent manner [4,8]. We hypothesized that the level of HGTD-P expression in gastric cancer cells would decrease or, if the tumors had increased HGTD-P expression, would be more vulnerable to cellular stress and cell death.…”

Section: Discussionmentioning

confidence: 99%

Expression and prognostic significance of human growth and transformation-dependent protein in gastric carcinoma and gastric adenoma

Cho

Kim

et al. 2009

Human Pathology

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mHGTD-P mediates hypoxic neuronal cell death via the release of apoptosis-inducing factor

Cited by 9 publications

References 22 publications

Proapoptotic Role of Human Growth and Transformation-Dependent Protein in the Developing Rat Brain After Hypoxia-Ischemia

Proapoptotic Role of Human Growth and Transformation-Dependent Protein in the Developing Rat Brain After Hypoxia-Ischemia

Caspase-9-Dependent Nuclear Translocation of Cytochrome <i>c</i> in Hypoxic Injury

Expression and prognostic significance of human growth and transformation-dependent protein in gastric carcinoma and gastric adenoma

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