Abstract
| Original language | English |
|---|---|
| Article number | 341 |
| Pages (from-to) | 341 |
| Journal | antioxidants |
| Volume | 8 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 24 Aug 2019 |
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Keywords
- vitamin D; oxidative stress; inflammation; retinal pigment epithelial cells; age-related macular degeneration
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Vitamin D Attenuates Oxidative Damage and Inflammation in Retinal Pigment Epithelial Cells. / Tohari, Ali Mohammad; Alhasani, Reem Hasaballah; Biswas, Lincoln; Patnaik, Sarita Rani ; Reilly, James; Zeng, Zhihong; Shu, Xinhua.
In: antioxidants, Vol. 8, No. 9, 341, 24.08.2019, p. 341.Research output: Contribution to journal › Article
TY - JOUR
T1 - Vitamin D Attenuates Oxidative Damage and Inflammation in Retinal Pigment Epithelial Cells
AU - Tohari, Ali Mohammad
AU - Alhasani, Reem Hasaballah
AU - Biswas, Lincoln
AU - Patnaik, Sarita Rani
AU - Reilly, James
AU - Zeng, Zhihong
AU - Shu, Xinhua
N1 - OA article Acceptance from webpage
PY - 2019/8/24
Y1 - 2019/8/24
N2 - Age-related macular degeneration (AMD), the most common visual disorder in elderly people, is characterized by the formation of deposits beneath the retinal pigment epithelium (RPE) and by dysfunction of RPE and photoreceptor cells. The biologically active form of vitamin D, 1,25-(OH)2D3 (VITD), is categorized as a multifunctional steroid hormone that modulates many transcriptional processes of different genes and is involved in a broad range of cellular functions. Epidemiological and genetic association studies demonstrate that VITD may have a protective role in AMD, while single nucleotide polymorphisms in the vitamin D metabolism gene (CYP24A1) increase the risk of AMD. However, the functional mechanisms of VITD in AMD are not fully understood. In the current study, we investigated the impact of VITD on H2O2-induced oxidative stress and inflammation in human RPE cells. We demonstrate that exposure to H2O2 caused significantly reduced cell viability, increased production of reactive oxygen species (ROS), lowered expression of antioxidant enzymes and enhanced inflammation. VITD exposure notably counteracted the above H2O2-induced effects. Our data suggest that VITD protects the RPE from oxidative damage and elucidate molecular mechanisms of VITD deficiency in the development of AMD.
AB - Age-related macular degeneration (AMD), the most common visual disorder in elderly people, is characterized by the formation of deposits beneath the retinal pigment epithelium (RPE) and by dysfunction of RPE and photoreceptor cells. The biologically active form of vitamin D, 1,25-(OH)2D3 (VITD), is categorized as a multifunctional steroid hormone that modulates many transcriptional processes of different genes and is involved in a broad range of cellular functions. Epidemiological and genetic association studies demonstrate that VITD may have a protective role in AMD, while single nucleotide polymorphisms in the vitamin D metabolism gene (CYP24A1) increase the risk of AMD. However, the functional mechanisms of VITD in AMD are not fully understood. In the current study, we investigated the impact of VITD on H2O2-induced oxidative stress and inflammation in human RPE cells. We demonstrate that exposure to H2O2 caused significantly reduced cell viability, increased production of reactive oxygen species (ROS), lowered expression of antioxidant enzymes and enhanced inflammation. VITD exposure notably counteracted the above H2O2-induced effects. Our data suggest that VITD protects the RPE from oxidative damage and elucidate molecular mechanisms of VITD deficiency in the development of AMD.
KW - vitamin D; oxidative stress; inflammation; retinal pigment epithelial cells; age-related macular degeneration
U2 - 10.3390/antiox8090341
DO - 10.3390/antiox8090341
M3 - Article
VL - 8
SP - 341
IS - 9
M1 - 341
ER -