Effect of glucosamine on premature senescence in hydrogen peroxide-treated human RPE cells
Therefore, we further investigated the effects of GlcN on H[sub]2O[sub]2-induced premature senescence in human RPE cells by SA-[sz]-Gal staining.
H[sub]2O[sub]2-induced premature senescence is due to the overexpression of the cyclin-dependent kinase inhibitor, p21 protein, in RPE cells.
The results of this study show that the occurrence of premature senescence in cotton plants at most of the studied sites is related to potassium availability in soils.
Premature senescence symptoms occur occasionally at the Narrabri site and it is possible that other factors such as soil compaction, waterlogging, and cool cloudy weather conditions may have caused the PS symptoms at the Narrabri site (Wright 1999).
Autophagy is required for suppressing the activation of the Nrf2-dependent stress response, maintaining the proliferative potential and preventing premature senescence of melanocytes.
Under oxidative stress, ROS produced in melanocytes could induce autophagy and activate the Nrf2 antioxidant pathway, remove toxic molecules, and maintain the redox homeostasis of melanocytes, while continuous stimulation of ROS might eventually lead to inactivation of autophagy and excessive activation of Nrf2 antioxidant pathway and break the redox homeostasis of melanocytes, resulting in premature senescence, decreased proliferation, and pigment synthesis, which may be involved in the onset of vitiligo.
Apart from oxidative stress, also other factors, like nonphysiological mechanical loading, an acidic environment, or autoimmune reactions, can alter the cellular phenotype and enhance premature senescence and cell death in the IVD [25, 32, 33].
The effect of EGCG (E4143, Sigma) on premature senescence was tested in three different experimental setups to identify mechanism of EGCG's action (Table 2): (1) to test its antioxidant activity, 10 [micro]M EGCG was applied in the stress phase simultaneously with [H.
Zinc finger protein 637 protects cells against oxidative stress-induced premature senescence by mtert-mediated telomerase activity and telomere maintenance," Cell Death & Disease, vol.
Hypoxia reoxygenation induces premature senescence in neonatal SD rat cardiomyocytes," Acta Pharmacologica Sinica, vol.
