The autophagy incidence was reduced from 30. 37 0. 95% to 20. 60 0. 79% after SKLB1002 cells were re fed with 10% FBS for six hours. There was no increase in apoptosis incidence in those AF cells. The mRNA expression of Beclin 1, Bcl 2, and LC3 was also evaluated. As expected, the levels of Beclin 1 and LC3 mRNA were significantly reduced by 10% FBS. The results were consistent with those shown by flow cyto metry. All these findings indicate that autop hagy Inhibitors,Modulators,Libraries can be rescued to some degree when cells are cultured with nutrient supplementation. Apoptosis increases with autophagy inhibition To investigate the interplay between autophagy and apoptosis in the AF cells, cells were treated Inhibitors,Modulators,Libraries with 3 MA, an autophagy inhibitor. Treatment with 3 MA significantly diminished the autophagy incidence, which was induced by 24 hour IL 1b treatment under serum deprivation in AF cells.
In contrast, 3 MA significantly increased the apoptosis incidence in AF cells under this experimental condition, Inhibitors,Modulators,Libraries shown by flow cytometry. The Hochest staining of apoptotic cells was also observed by using a phase con trast microscopy. The results suggest that the inhibition of autophagy does trigger apoptosis in the AF cells. Discussion In the current study, we confirmed that, for the first time, autophagy takes place in AF cells as shown by evi dence from electronic microscopy and immunofluores cence examination. To the best of our knowledge, this is the first report of autophagy in AF cells. Our results suggest that IL 1b does not induce autophagy in AF cells by itself, but it augments the autophagy induced by serum deprivation.
No morphological changes were observed Inhibitors,Modulators,Libraries by microscopy during the autophagy process. Our study also shows that the inhibition of autophagy in AF cells is accompanied by a significant increase in the apoptosis incidence. On the other hand, autophagic AF cells could be rescued by re feeding with FBS. These results demonstrate Inhibitors,Modulators,Libraries that autophagy partially protects AF cells from apoptosis, when AF cells face the stimulation of IL 1b and serum deprivation. During IVD degenera tion, both the annulus fibrosus and Deltarasin? the nucleus suffer from insufficient nutrient supply and local increase of IL 1b. Thus, these findings indicate that autop hagy may play an important role in the pathogenesis of IVD degeneration. Recent studies have documented autophagy in articu lar cartilage. Bohensky et al, based on their experi ments, suggested that autophagy could be induced in chondrocytes and regulated by hypoxia inducible factor family. Almonte Becerril et al. concluded that both apoptosis and autophagy were observed in chondrocytes during pathological process of osteoarthritis. Car ams et al.
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