Expression by cells of the SA-beta-Gal was shown to be a reliable indicator of the switch mechanism used by cells to enter the senescent phenotype. We used this method in order to explore the variation of SA-beta-Gal-positive cells with passage number and time spent in culture. Both parameters produced an increase of SA-beta-Gal-positive cells. The addition of a Maillard-product (advanced glycation end-product=AGE) to the fibroblast cultures also increased SA-beta-Gal expression. Fucose- and rhamnose-rich oligo- and polysaccharides (FROPs and RROPs, respectively) provided a significant protection against this AGE-induced increase of SA-beta-Gal-positive cells. It is speculated that these processes might well play an important role in skin aging.
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http://dx.doi.org/10.1016/j.archger.2007.12.004 | DOI Listing |
Exp Dermatol
January 2025
Department of Dermatology, Ajou University School of Medicine; Suwon, Suwon, Korea.
Senescent melanocytes have been suggested to play a role in the development of ageing-associated pigmentary changes and skin ageing. Here, we assessed the senolytic capacity of recognised senolytic chemicals and natural compounds in UV-irradiated senescent melanocytes. Among the tested agents, only ABT-737 and ABT-263 showed a significant reduction in the number of SA-β-Gal-positive senescent melanocytes and in the expressions of p16 and p21.
View Article and Find Full Text PDFHum Cell
January 2025
Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.
Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.
View Article and Find Full Text PDFBiofactors
January 2025
Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung, Taiwan, ROC.
Ultraviolet (UV) irradiation is a major factor contributing to skin photoaging, including the formation of reactive oxygen species (ROS), collagen breakdown, and overall skin damage. Insulin-like growth factor-I (IGF-1) is a polypeptide hormone that regulates dermal survival and collagen synthesis. Echinacoside (Ech), a natural phenylethanoid glycoside, is the most abundant active compound in Cistanches.
View Article and Find Full Text PDFEnviron Health Prev Med
January 2025
Health and Environmental Risk Division, National Institute for Environmental Studies.
Background: Chronic arsenite exposure has been known to induce cancer in various organs; however, the underlying mechanisms remain elusive. The characteristic feature of carcinogenesis due to arsenic exposure is that the disease develops after a prolonged latent period, even after cessation of exposure. Our previous study revealed that arsenite exposure induces premature senescence in hepatic stellate cells and suggests that the senescence-associated secretory phenotype (SASP) factors from the senescent cells promote hepatic carcinogenesis.
View Article and Find Full Text PDFExp Neurol
December 2024
School of Life Sciences, Lanzhou University, Lanzhou 730000, Gansu Province, China. Electronic address:
Various factors and mechanisms, including radiation, initiate cellular senescence and are concurrent with the progression of various neurodegenerative diseases. Radiation-induced chromosomal aberrations and DNA integrity damage impact the processes of cellular growth, maturation, and aging. Astragaloside IV (AS-IV) has been documented to display significant neuroprotective effects on inflammation, oxidative stress, and cellular apoptosis; however, the precise neuroprotective mechanism of AS-IV against neuronal aging remains unclear.
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