Linked Life Data

1946415

Source:http://linkedlifedata.com/resource/pubmed/id/1946415

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
1991-12-3
pubmed:abstractText
Hypoxemia is associated with a prothrombotic tendency. In this study we report the purification and partial characterization of an activator of a central coagulation component, factor X, induced in endothelium by exposure to hypoxia (hypoxia-induced factor X activator or Xact). Expression of Xact occurred in a reversible manner when endothelial cell cultures were exposed to hypoxia or sodium azide but not in response to a variety of other alterations in the cellular milieu, such as heat shock or glucose deprivation. The activity of Xact, which was not detected in normoxic endothelial cells, was maximal under acidic conditions, pH 6.0-6.8, which often coexist with hypoxia in an ischemic milieu. By sequential isoelectric focusing and preparative SDS/PAGE of endothelial membrane-rich fractions, Xact was purified approximately 19,000-fold and found to be a single-chain, approximately 100-kDa polypeptide with pI approximately 5.0. Activation of factor X by purified Xact was not affected by blocking antibodies to other coagulation proteins or by phenylmethylsulfonyl fluoride or leupeptin but was prevented by mercury chloride or iodoacetamide. In addition to the induction of Xact, two-dimensional gel analysis of membrane fractions from metabolically labeled hypoxic endothelial cultures revealed two groups of approximately 10 additional spots: (i) a group for which expression was maximal after 24 hr and (ii) a group for which expression continued to increase up to 48 hr. The pattern of hypoxia-mediated modulation of protein expression was distinct from that seen with other cellular stimuli but could be duplicated, in part, by sodium azide. These results indicate that hypoxia elicits a specific biosynthetic response, including the expression of endothelial cell-surface molecules that can alter cellular function and may potentially serve as markers of hypoxemic vessel-wall injury.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-2156893, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-236308, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-2617454, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-2768244, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-2925693, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-3198758, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-3283153, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-3510555, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-3594745, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-3935163, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-434458, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-4796071, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-489550, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-5432063, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-6099581, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-7470818, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946415-925006
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9897-901
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Hypoxia induces endothelial cell synthesis of membrane-associated proteins.
pubmed:affiliation
Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't