Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-7-15
pubmed:abstractText
Myeloid leukocytes are thought to regulate their susceptibility to apoptosis upon migration to a site of inflammation. However, factors that determine survival have not been well characterized in these cells. We have examined the expression of murine A1, an antiapoptotic Bcl-2 relative found in activated myeloid cells, during the course of an acute inflammatory response. Intraperitoneal infection of mice with the virulent RH strain of Toxoplasma gondii led to a 5- to 10-fold increase in A1 mRNA levels in peritoneal cells after several days. Bcl-2 expression was unchanged. The increase in A1 expression depended on the dose of the organism and coincided with a sharp increase in peritoneal cellularity. A1 protein levels were also increased as determined by Western blot analysis and immunohistochemical studies. All neutrophils and approximately half of the macrophages in the inflammatory exudate contained high levels of A1 in cytoplasm. A1 expression did not correlate with intracellular parasitization. Peripheral blood neutrophils from normal mice strongly expressed A1 protein, whereas normal monocytes showed only weak staining. Bax mRNA was induced in parallel with A1 in macrophages. Exudate macrophages and granulocytes that were apoptotic by TUNEL staining occasionally appeared to display A1 throughout the cell nucleus. These studies identify A1 as a potential regulator of apoptosis during acute inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/BCL2-related protein A1, http://linkedlifedata.com/resource/pubmed/chemical/Bax protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins, http://linkedlifedata.com/resource/pubmed/chemical/MATA1 protein, S cerevisiae, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Replication Protein C, http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Saccharomyces cerevisiae Proteins, http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
412-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10384143-Animals, pubmed-meshheading:10384143-Apoptosis, pubmed-meshheading:10384143-DNA-Binding Proteins, pubmed-meshheading:10384143-Female, pubmed-meshheading:10384143-Homeodomain Proteins, pubmed-meshheading:10384143-Inflammation, pubmed-meshheading:10384143-Macrophages, pubmed-meshheading:10384143-Mice, pubmed-meshheading:10384143-Mice, Inbred BALB C, pubmed-meshheading:10384143-Neutrophils, pubmed-meshheading:10384143-Peritoneal Cavity, pubmed-meshheading:10384143-Proto-Oncogene Proteins, pubmed-meshheading:10384143-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:10384143-RNA, Messenger, pubmed-meshheading:10384143-Replication Protein C, pubmed-meshheading:10384143-Repressor Proteins, pubmed-meshheading:10384143-Saccharomyces cerevisiae Proteins, pubmed-meshheading:10384143-Subcellular Fractions, pubmed-meshheading:10384143-Toxoplasma, pubmed-meshheading:10384143-Toxoplasmosis, Animal, pubmed-meshheading:10384143-bcl-2-Associated X Protein
pubmed:year
1999
pubmed:articleTitle
The murine antiapoptotic protein A1 is induced in inflammatory macrophages and constitutively expressed in neutrophils.
pubmed:affiliation
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. orlofsky@aecom.yu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.