Linked Life Data

9367881

Source:http://linkedlifedata.com/resource/pubmed/id/9367881

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-12-15
pubmed:abstractText
We have shown previously that intracellular Ca+2 chelation and calpain inhibitors block the influx of extracellular Ca+2 and Cl- during the late phase of cell injury in renal proximal tubules (RPT) exposed to the mitochondrial inhibitor antimycin A. Since the endoplasmic reticulum (ER) is the major intracellular Ca+2 storage site, ER Ca+2 release/depletion may mediate the Ca+2 influx and cell death. Treatment of RPT suspensions with thapsigargin, an ER Ca+2-ATPase inhibitor, increased cytosolic free Caf+2 (Ca+2) levels from 122 +/- 7 to 322 +/- 55 nM within 10 sec of addition followed by a return to control levels within 3 min. A 5-min pretreatment of RPT suspensions with thapsigargin blocked antimycin A- and hypoxia-induced influx of extracellular Ca+2 and Cl- and the resulting cell death/lysis. These data suggest that ER Ca+2 release/depletion during cell injury may trigger a signaling cascade that causes extracellular Ca+2 influx followed by Cl- influx, cell swelling, and ultimately cell death/ lysis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
240
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
57-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Depletion of endoplasmic reticulum calcium stores protects against hypoxia- and mitochondrial inhibitor-induced cellular injury and death.
pubmed:affiliation
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205-7199, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't