Genomic profiling of restraint stress-induced alterations in mouse T lymphocytes.
DNA damage-, DNA repair-, and apoptosis-related gene expression in CD3(+) T lymphocytes of BALB/c mice subjected to 2-h restraint stress were compared to that in CD3(+)T lymphocytes from control mice. Using targeted cDNA arrays, significant increases in expression of genes serving as sensors of DNA damage, including MSH genes and RAD53, were observed. GADD45g, a gene responsible for regulating cell cycle arrest and apoptosis, was significantly induced; as was Pura, a gene involved in cell proliferation. These data suggest that, at the molecular level, stress activates genes responsible for priming the T cell to either undergo apoptosis or proliferation.
Flint
Melanie S
MS
University of Pittsburgh Cancer Institute and Department of Psychology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. flintms@upmc.edu
Carroll
Judith E
JE
Jenkins
Frank J
FJ
Chambers
William H
WH
Han
Melissa L
ML
Baum
Andrew
A
D000818:Animals; D049109:Cell Proliferation; D020552:Comet Assay / Q000379:methods; D003345:Corticosterone / Q000378:metabolism; D004249:DNA Damage / Q000502:physiology; D005260:Female; D005434:Flow Cytometry / Q000379:methods; D015870:Gene Expression / Q000502:physiology*; D020869:Gene Expression Profiling; D051379:Mice; D008807:Mice, Inbred BALB C; D008954:Models, Biological; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D012333:RNA, Messenger / Q000096:biosynthesis; D012149:Restraint, Physical / Q000379:methods; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013312:Stress, Physiological / Q000235:genetics / Q000378:metabolism*; D013601:T-Lymphocytes / Q000378:metabolism*; D013997:Time Factors
D012333:RNA, Messenger; D003345:Corticosterone