Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The epidermis is characterized by the continual turnover of its basic cellular unit, the keratinocyte. To determine whether genes known to regulate apoptosis could affect keratinocyte biology, transgenic mice overexpressing bcl-xL or bcl-xS under the control of the human keratin 14 promoter were generated. The maturation process and cellularity of the stratified epidermis were not compromised in the transgenic mice. Transgene function was demonstrated by enhanced cell survival of bcl-xL transgenic versus wild-type primary keratinocyte cultures treated with etoposide. To test the response of these mice to genotoxic damage, wild-type and transgenic mice were irradiated with UV light. The bcl-xL transgenic mice showed a dramatically increased resistance to irradiation, whereas the bcl-xS transgenic mice showed an increased sensitivity to irradiation. In contrast, neither transgene influenced the rate of would repair. Interestingly, endogenous Bcl-x was rapidly induced in keratinocytes adjacent to the would. Taken together, these findings demonstrate that although the terminal differentiation program is not altered by Bcl-x, acute stress responses within the skin can be influenced by regulators of apoptosis such as Bcl-x.
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PMID:Bcl-x expression influences keratinocyte cell survival but not terminal differentiation. 918 96

To test the hypothesis that the aging mammalian heart and brain might have increased vulnerability to acute stress, DNA fragmentation was studied after hypoxia-reoygenation in young adult (6 months) and old (22-24 months) F344 rats. Heart and brain tissue were examined at the following time points: 30, 60, or 90 min of hypoxia (H, 5% O2, 95% N2) plus 2 h of reoxygenation (R, room air, 21% O2). With increasing duration of hypoxia preceding the reoxygenation, the extent of DNA fragmentation (in situ terminal dUTP nick end labeling, TUNEL, positive cells) was progressively higher in both age groups, greater in the old compared to that of the young adult rat. The levels of the anti-apoptotic proteins bcl-2 and bcl-xL, were similar in young and old at baseline and tended to increase in both age groups after hypoxia/reoxygenation. The pro-apoptotic protein, bax, was higher at baseline in the old; it rose after hypoxia/reoxygenation in the young adult heart and brain, but was unchanged in the old heart and was decreased in the old brain. The ratios of bcl-2/bax and of bcl-xL/bax were higher in the old heart and brain compared to that in the young adult after hypoxia/reoxygenation. Thus, compared to that of the young adult, the heart and brain of the old rat have lower thresholds and are more vulnerable to injury induced by hypoxia/reoxygenation, despite rapid and heightened expression of the anti-apoptotic proteins bcl-2 and bcl-xl. This could be due partly to the age-associated increase in the basal expression of the pro-apoptotic protein bax, as well as possibly other factors.
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PMID:Influence of age on hypoxia/reoxygenation-induced DNA fragmentation and bcl-2, bcl-xl, bax and fas in the rat heart and brain. 1065 80