Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-5-9
pubmed:abstractText
Major physical traumas provoke a systemic inflammatory response and immune dysfunction. In a model of thermal injury in rats, we previously showed that an overproduction of nitric oxide (NO) was responsible for the collapse of lymphoproliferative responses. In the present work, we performed a time-course analysis of cell proliferation and cell death parameters in order to establish the sequence of events triggered by the high NO output in Wistar/Han rat splenocytes activated with Con A, 10 days after burn injury. We demonstrate that activated T cells from burned rats never divided whereas normal T cells underwent four division cycles. However, T cells from both burned and normal rat entered the G1 phase as shown by increase of cell size, mitochondria hyperpolarization, and expression of cyclin D1. Burned rat T cells progressed to the late G1 phase as shown by expression of the nuclear Ki-67 antigen, but they never entered the S phase. They underwent apoptosis as shown by morphological parameters, disruption of transmembrane mitochondrial potential, and DNA fragmentation. Persistent accumulation of the p53 protein accompanied these phenomena. NO synthase inhibitors antagonize alterations of cell proliferation and cell death parameters in burned rat T cells and accelerated p53 turnover.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-4827
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
306
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
150-67
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15878341-Animals, pubmed-meshheading:15878341-Apoptosis, pubmed-meshheading:15878341-Burns, pubmed-meshheading:15878341-Cell Division, pubmed-meshheading:15878341-Cell Proliferation, pubmed-meshheading:15878341-Concanavalin A, pubmed-meshheading:15878341-Enzyme Inhibitors, pubmed-meshheading:15878341-Flow Cytometry, pubmed-meshheading:15878341-G1 Phase, pubmed-meshheading:15878341-Interleukin-2, pubmed-meshheading:15878341-Isothiuronium, pubmed-meshheading:15878341-Lymphocyte Activation, pubmed-meshheading:15878341-Male, pubmed-meshheading:15878341-Models, Biological, pubmed-meshheading:15878341-Necrosis, pubmed-meshheading:15878341-Nitric Oxide, pubmed-meshheading:15878341-Rats, pubmed-meshheading:15878341-Rats, Wistar, pubmed-meshheading:15878341-Spleen, pubmed-meshheading:15878341-T-Lymphocytes, pubmed-meshheading:15878341-Thiazines, pubmed-meshheading:15878341-Tumor Suppressor Protein p53
pubmed:year
2005
pubmed:articleTitle
High levels of endogenous nitric oxide produced after burn injury in rats arrest activated T lymphocytes in the first G1 phase of the cell cycle and then induce their apoptosis.
pubmed:affiliation
Laboratoire de Physiologie Respiratoire, Faculté de Médecine Cochin/Port-Royal, Université Paris V, 24 rue du Faubourg Saint Jacques, 75014 Paris, France. valentilio@yahoo.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't