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Calcium-independent phospholipase A2...

Kinsey, Gilbert Roland.

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Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells./
作者:	Kinsey, Gilbert Roland.
面頁冊數:	188 p.
附註:	Adviser: Rick G. Schnellmann.
Contained By:	Dissertation Abstracts International68-05B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3263321
ISBN:	9780549012535

Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells.
Kinsey, Gilbert Roland.

Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells. - 188 p.

Adviser: Rick G. Schnellmann.

Thesis (Ph.D.)--Medical University of South Carolina, 2007.

Taken together these data suggest that manipulation of iPLA2gamma activity in renal cells may represent new potential therapies to prevent renal cell death that leads to acute renal failure.

ISBN: 9780549012535Subjects--Topical Terms:

1017686
Biology, Cell.

Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells.
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100 1 $a Kinsey, Gilbert Roland. $3 1270467
245 1 0 $a Calcium-independent phospholipase A2 gamma (iPLA2gamma): Intracellular localization and role in mitochondrial dysfunction, cell viability and oxidant-induced death in renal cells.
300 $a 188 p.
500 $a Adviser: Rick G. Schnellmann.
500 $a Source: Dissertation Abstracts International, Volume: 68-05, Section: B, page: 3007.
502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2007.
520 $a Taken together these data suggest that manipulation of iPLA2gamma activity in renal cells may represent new potential therapies to prevent renal cell death that leads to acute renal failure.
520 $a Rabbit renal proximal tubular cells (RPTC) possess significant calcium-independent phospholipase A2 (IPLA2) activity which is hypothesized to participate in lipid peroxidation repair. A role for RPTC IPLA2 in mediating non-oxidant induced apoptosis has been suggested. Major unanswered questions regarding RPTC IPLA2 were its identity and intracellular localization in RPTC, its role in mitochondrial dysfunction and the consequences of decreasing its expression in RPTC.
520 $a Mitochondrial IPLA2 activity in RPTC was demonstrated and characterized in terms of inhibitor sensitivity, substrate specificity, pH and ATP dependence. The endoplasmic reticulum (ER) and mitochondria) IPLA 2 activity in RPTC was sensitive to racemic bromoenol lactone (BEL) and R-BEL but not methyl arachidonyl fluorophosphonate or arachidonyl trifluoromethylketone or S-BEL. This sensitivity profile is consistent with iPLA2gamma and no other PLA2 isoform. Reverse transcriptase-polymerase chain reaction demonstrated the presence of iPLA2gamma, and not iPLA 2beta, mRNA in RKC. Immunoblot analysis confirmed the expression of iPLA2gamma in RPTC ER and mitochondria. In summary, ER and mitochondria) iPLA2 in RPTC was determined to be iPLA2gamma.
520 $a Divergent roles for iPLA2gamma during oxidative stress and Ca2+-induced mitochondria) permeability transition (MPT) in renal cortex mitochondria (RCM) were determined. Oxidant-mediated lipid peroxidation and mitochondrial swelling were accelerated in RCM by selective IPLA 2gamma inhibition. Conversely, IPLA2gamma inhibition delayed opening of the MPT pore in RCM by reducing the generation of arachidonic acid. These results suggest that mitochondrial IPLA2gamma plays different roles depending on the type of injury; participating in repair of oxidant-mediated lipid peroxidation and mediating non-oxidant-induced dysfunction.
520 $a Adenoviral shRNA-mediated knock-down of ER and mitochondrial iPLA 2gamma in RPTC resulted in increased lipid peroxidation, decreased mitochondrial function and eventually apoptotic cell death in the absence of toxicant exposure. Furthermore, iPLA2gamma knockdown sensitized RPTC to non-lethal doses of a model oxidant tert-butyl hydroperoxide (TBHP) and selective iPLA2gamma inhibition with R-BEL potentiated TBHP-induced necrosis. In summary, decreasing iPLA2gamma protein expression confirms that this enzyme is required for repair of lipid peroxidation and maintenance of RPTC viability.
590 $a School code: 0122.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Health Sciences, Toxicology. $3 1017752
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710 2 $a Medical University of South Carolina. $3 700119
773 0 $t Dissertation Abstracts International $g 68-05B.
790 $a 0122
790 1 0 $a Schnellmann, Rick G., $e advisor
791 $a Ph.D.
792 $a 2007
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