scholarly journals Pharmacological inhibition of mitochondrial fission attenuates oxidative stress-induced damage of retinal pigmented epithelial cells

2021 ◽  
Vol 146 (3) ◽  
pp. 149-159
Author(s):  
Tomohiro Yako ◽  
Maho Nakamura ◽  
Shinsuke Nakamura ◽  
Hideaki Hara ◽  
Masamitsu Shimazawa
2011 ◽  
Vol 52 (2) ◽  
pp. 890 ◽  
Author(s):  
Gerard A. Rodrigues ◽  
Florence Maurier-Mahé ◽  
Dixie-Lee Shurland ◽  
Anne Mclaughlin ◽  
Keith Luhrs ◽  
...  

2007 ◽  
Vol 282 (31) ◽  
pp. 22414-22425 ◽  
Author(s):  
Zhihao Wu ◽  
Thomas W. Lauer ◽  
Anna Sick ◽  
Sean F. Hackett ◽  
Peter A. Campochiaro

2021 ◽  
Vol 12 ◽  
Author(s):  
Francesca Lazzara ◽  
Federica Conti ◽  
Chiara Bianca Maria Platania ◽  
Chiara M. Eandi ◽  
Filippo Drago ◽  
...  

Age-related macular degeneration (AMD) is a degenerative retinal disease and one of major causes of irreversible vision loss. AMD has been linked to several pathological factors, such as oxidative stress and inflammation. Moreover, Aβ (1–42) oligomers have been found in drusen, the extracellular deposits that accumulate beneath the retinal pigmented epithelium in AMD patients. Hereby, we investigated the hypothesis that treatment with 1,25(OH) 2D3 (vitamin D3) and meso-zeaxathin, physiologically present in the eye, would counteract the toxic effects of three different insults on immortalized human retinal pigmented epithelial cells (ARPE-19). Specifically, ARPE-19 cells have been challenged with Aβ (1–42) oligomers, H2O2, LPS, and TNF-α, respectively. In the present study, we demonstrated that the combination of 1,25(OH)2D3 and meso-zeaxanthin significantly counteracted the cell damage induced by the three insults, at least in these in vitro integrated paradigms of AMD. These results suggest that combination of 1,25(OH)2D3 and meso-zeaxathin could be a useful approach to contrast pathological features of AMD, such as retinal inflammation and oxidative stress.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Xiao-Chun Sun ◽  
Yue Wang ◽  
Han-Fang Zeng ◽  
Yu-Meng Xi ◽  
Hong Lin ◽  
...  

AbstractWith global warming, heat stress has become an important challenge for the global dairy industry. Sirtuin 3 (SIRT3), an important mitochondrial NAD+dependent decarboxylase and a major regulator of cellular energy metabolism and antioxidant defense, is integral to maintaining normal mitochondrial function. The aim of this study was to assess the protective effect of SIRT3 on damage to bovine mammary epithelial cells (BMECs) induced by heat stress and to explore its potential mechanism. Our results indicate that SIRT3 is significantly downregulated in heat-stressed mammary tissue and high-temperature-treated BMECs. SIRT3 knockdown significantly increased the expression of HSP70, Bax, and cleaved-caspase 3 and inhibited the production of antioxidases, thus promoting ROS production and cell apoptosis in BMECs. In addition, SIRT3 knockdown can aggravate mitochondrial damage by mediating the expression of genes related to mitochondrial fission and fusion, including dynamin-related protein 1, mitochondrial fission 1 protein, and mitochondrial fusion proteins 1and 2. In addition, SIRT3 knockdown substantially decreased AMPK phosphorylation in BMECs. In contrast, SIRT3 overexpression in high-temperature treatment had the opposite effect to SIRT3 knockdown in BMECs. SIRT3 overexpression reduced mitochondrial damage and weakened the oxidative stress response of BMECs induced by heat stress and promoted the phosphorylation of AMPK. Taken together, our results indicate that SIRT3 can protect BMECs from heat stress damage through the AMPK signaling pathway. Therefore, the reduction of oxidative stress by SIRT3 may be the primary molecular mechanism underlying resistance to heat stress in summer cows.


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