AI Article Synopsis
- The study aimed to explore how STAT3 changes during cell aging (replicative senescence) and the impact of angiotensin II (AngII) on STAT3 activity.
- Researchers used a normal fetal lung cell line (WI-38) and identified senescent cells through beta-gal staining, while employing assays to assess STAT3 activation levels.
- Findings indicated that while STAT3 protein levels increased during aging cells, its ability to translocate to the nucleus and bind DNA decreased, and AngII stimulated STAT3 less effectively in senescent cells compared to mature cells.
Article Abstract
Objective: To investigate the changes of STAT3 in cell replicative senescence and the effects of angiotensin II (AngII) on STAT3.
Methods: Normal human fetal lung diploid fibroblast cell line WI-38 was cultured and the senescent cell was defined with beta-gal staining. Electrophoretic mobility shift assay and Western blotting assay were used to detect the activation of STAT3 during cell replicative senescence and examine the process of STAT3 activation with AngII.
Results: The synthesis of STAT3 protein during the course of cell replicative senescent increased, the nuclear translocation of phosphorylated STAT3 decreased, and the activities of STAT3 binding DNA reduced.
Conclusion: AngII induces the activation of STAT3 in both mature and senescence cell by AT(1) receptor, however, the reaction of senescent cell to AngII is weaker. The site of block may be in the nuclear translocation. AngII induces the activity of STAT3 in replicative senescence WI-38.
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