CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells
Diabetic retinopathy (DR) is one of the most common diabetic complications and remains the leading cause of vision loss among adults. C1q/TNF-related protein 3 (CTRP3) is a member of CTRP family that has been found to be involved in the progression of diabetes mellitus and diabetic complications. Ho...
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Taylor & Francis Group
2019-12-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2019.1666864 |
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| author | Jian Zhang Jing He |
| author_facet | Jian Zhang Jing He |
| author_sort | Jian Zhang |
| collection | DOAJ |
| description | Diabetic retinopathy (DR) is one of the most common diabetic complications and remains the leading cause of vision loss among adults. C1q/TNF-related protein 3 (CTRP3) is a member of CTRP family that has been found to be involved in the progression of diabetes mellitus and diabetic complications. However, the role of CTRP3 in DR has not been fully understood. In the present study, the results showed that CTRP3 expression was significantly decreased in DR patients compared with controls. In vitro investigations proved that overexpression of CTRP3 improved cell viability of ARPE-19 cells in response to high glucose (HG) stimulation. CTRP3 also attenuated HG-induced oxidative stress in ARPE-19 cells with decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased superoxide dismutase (SOD) activity. Apoptotic rate was significantly decreased in CTRP3 overexpressing ARPE-19 cells. Besides, bcl-2 expression was increased, while bax expression was decreased by CTRP3 overexpression. Moreover, overexpression of CTRP3 enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) pathway in HG-stimulated ARPE-19 cells, and Nrf2 knockdown reversed CTRP3-mediated oxidative stress and apoptosis. These findings suggested that CTRP3 attenuated HG-stimulated oxidative stress and apoptosis in ARPE-19 cells, which were mediated by activation of Nrf2/HO-1 pathway. |
| format | Article |
| id | doaj-art-f0c48bb9975f441faa7cbda656ece903 |
| institution | Matheson Library |
| issn | 2169-1401 2169-141X |
| language | English |
| publishDate | 2019-12-01 |
| publisher | Taylor & Francis Group |
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| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj-art-f0c48bb9975f441faa7cbda656ece9032025-07-21T21:22:48ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014713758376410.1080/21691401.2019.1666864CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cellsJian Zhang0Jing He1Department of Ophthalmology, Shaanxi Provincial People’s Hospital, Xi’an, ChinaDepartment of Obstetrics, First Affiliated Hospital of Xi’an Medical College, Xi’an, ChinaDiabetic retinopathy (DR) is one of the most common diabetic complications and remains the leading cause of vision loss among adults. C1q/TNF-related protein 3 (CTRP3) is a member of CTRP family that has been found to be involved in the progression of diabetes mellitus and diabetic complications. However, the role of CTRP3 in DR has not been fully understood. In the present study, the results showed that CTRP3 expression was significantly decreased in DR patients compared with controls. In vitro investigations proved that overexpression of CTRP3 improved cell viability of ARPE-19 cells in response to high glucose (HG) stimulation. CTRP3 also attenuated HG-induced oxidative stress in ARPE-19 cells with decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased superoxide dismutase (SOD) activity. Apoptotic rate was significantly decreased in CTRP3 overexpressing ARPE-19 cells. Besides, bcl-2 expression was increased, while bax expression was decreased by CTRP3 overexpression. Moreover, overexpression of CTRP3 enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) pathway in HG-stimulated ARPE-19 cells, and Nrf2 knockdown reversed CTRP3-mediated oxidative stress and apoptosis. These findings suggested that CTRP3 attenuated HG-stimulated oxidative stress and apoptosis in ARPE-19 cells, which were mediated by activation of Nrf2/HO-1 pathway.https://www.tandfonline.com/doi/10.1080/21691401.2019.1666864Diabetic retinopathy (DR)C1q/TNF-related protein 3 (CTRP3)high glucose (HG)oxidative stressNrf2/HO-1 pathway |
| spellingShingle | Jian Zhang Jing He CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells Artificial Cells, Nanomedicine, and Biotechnology Diabetic retinopathy (DR) C1q/TNF-related protein 3 (CTRP3) high glucose (HG) oxidative stress Nrf2/HO-1 pathway |
| title | CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| title_full | CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| title_fullStr | CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| title_full_unstemmed | CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| title_short | CTRP3 inhibits high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| title_sort | ctrp3 inhibits high glucose induced oxidative stress and apoptosis in retinal pigment epithelial cells |
| topic | Diabetic retinopathy (DR) C1q/TNF-related protein 3 (CTRP3) high glucose (HG) oxidative stress Nrf2/HO-1 pathway |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2019.1666864 |
| work_keys_str_mv | AT jianzhang ctrp3inhibitshighglucoseinducedoxidativestressandapoptosisinretinalpigmentepithelialcells AT jinghe ctrp3inhibitshighglucoseinducedoxidativestressandapoptosisinretinalpigmentepithelialcells |