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PubMed:23582235 JSONTXT

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PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 161-679 OBJECTIVE denotes Pathological release of excess zinc ions has been implicated in ischemic brain cell death. However, the underlying mechanisms remain to be elucidated. In stroke, ischemia-induced zinc release and hypoxia-inducible factor-1 (HIF-1) accumulation concurrently occur in the ischemic tissue. The present study tests the hypothesis that the presence of high intracellular zinc concentration is a major cause of modifications to PARP-1 and HIF-1α during hypoxia, which significantly contributes to cell death during ischemia.
T2 689-924 METHODS denotes Primary cortical astrocytes and C8-D1A cells were exposed to different concentrations of zinc chloride. Cell death rate and protein expression of HIF-1 and Poly(ADP-ribose) polymerase (PARP)-1 were examined after 3-h hypoxic treatment.
T3 934-1521 RESULTS denotes Although 3-h hypoxia or 100 μM of zinc alone did not induce noticeable cytotoxicity, their combination led to a dramatic increase in astrocytic cell death in a zinc-concentration-dependent manner. Exposure of astrocytes to hypoxia for 3 h remarkably increased the levels of intracellular zinc and HIF-1α protein, which was further augmented by added exogenous zinc. Notably, HIF-1α knockdown blocked zinc-induced astrocyte death. Moreover, knockdown of PARP-1, another important protein in the response of hypoxia, attenuated the overexpression of HIF-1α and reduced the cell death rate.
T4 1535-1780 CONCLUSIONS denotes Our studies show that zinc promotes hypoxic cell death through overexpression of the hypoxia response factor HIF-1α via the cell fate determine factor PARP-1 modification, which provides a novel mechanism for zinc-mediated ischemic brain injury.

Allie

Id Subject Object Predicate Lexical cue
SS1_23582235_4_0 357-383 expanded denotes hypoxia-inducible factor-1
SS2_23582235_4_0 385-390 abbr denotes HIF-1
SS1_23582235_8_0 845-872 expanded denotes Poly(ADP-ribose) polymerase
SS2_23582235_8_0 874-878 abbr denotes PARP
AE1_23582235_4_0 SS1_23582235_4_0 SS2_23582235_4_0 abbreviatedTo hypoxia-inducible factor-1,HIF-1
AE1_23582235_8_0 SS1_23582235_8_0 SS2_23582235_8_0 abbreviatedTo Poly(ADP-ribose) polymerase,PARP

PubmedHPO

Id Subject Object Predicate Lexical cue
T1 315-321 HP_0001297 denotes stroke

CHEMDNER-training-test

Id Subject Object Predicate Lexical cue
T1 192-196 SYSTEMATIC denotes zinc
T2 340-344 SYSTEMATIC denotes zinc
T3 527-531 SYSTEMATIC denotes zinc
T4 778-791 SYSTEMATIC denotes zinc chloride
T5 845-861 SYSTEMATIC denotes Poly(ADP-ribose)
T6 968-972 SYSTEMATIC denotes zinc
T7 1094-1098 SYSTEMATIC denotes zinc
T8 1222-1226 SYSTEMATIC denotes zinc
T9 1294-1298 SYSTEMATIC denotes zinc
T10 1334-1338 SYSTEMATIC denotes zinc
T11 1557-1561 SYSTEMATIC denotes zinc
T12 1744-1748 SYSTEMATIC denotes zinc
T1 0-4 SYSTEMATIC denotes Zinc
T2 132-861 SYSTEMATIC denotes P-ribose) polymerase-1. AIM: Pathological release of excess zinc ions has been implicated in ischemic brain cell death. However, the underlying mechanisms remain to be elucidated. In stroke, ischemia-induced zinc release and hypoxia-inducible factor-1 (HIF-1) accumulation concurrently occur in the ischemic tissue. The present study tests the hypothesis that the presence of high intracellular zinc concentration is a major cause of modifications to PARP-1 and HIF-1α during hypoxia, which significantly contributes to cell death during ischemia. METHODS: Primary cortical astrocytes and C8-D1A cells were exposed to different concentrations of zinc chloride. Cell death rate and protein expression of HIF-1 and Poly(ADP-ribose)