Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions
AIM: To investigate biological effects of transthyretin (TTR) on the development of neovascularization under simulated diabetic retinopathy (DR) condition associated with high glucose and hypoxia. METHODS: Human retinal microvascular endothelial cells (hRECs) were cultured in normal and simulated D...
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| Format: | Article |
| Language: | English |
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Press of International Journal of Ophthalmology (IJO PRESS)
2016-06-01
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| Series: | International Journal of Ophthalmology |
| Subjects: | |
| Online Access: | http://www.ijo.cn/en_publish/2016/6/20160603.pdf |
| _version_ | 1818024035867426816 |
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| author | Jun Shao Yong Yao |
| author_facet | Jun Shao Yong Yao |
| author_sort | Jun Shao |
| collection | DOAJ |
| description | AIM: To investigate biological effects of transthyretin (TTR) on the development of neovascularization under simulated diabetic retinopathy (DR) condition associated with high glucose and hypoxia.
METHODS: Human retinal microvascular endothelial cells (hRECs) were cultured in normal and simulated DR environments with high glucose and hypoxia. The normal serum glucose concentration is approximately 5.5 mmol/L; thus, hyperglycemia was simulated with 25 mmol/L glucose, while hypoxia was induced using 200 µmol/L CoCl2. The influence of TTR on hRECs and human retinal pigment epithelial cells (hRPECs) was determined by incubating the cells with 4 μmol/L TTR in normal and abnormal media. A co-culture system was then employed to evaluate the effects of hRPECs on hRECs.
RESULTS: Decreased hRECs and hRPECs were observed under abnormal conditions, including high-glucose and hypoxic media. In addition, hRECs were significantly inhibited by 4 μmol/L exogenous TTR during hyperglycemic culture. During co-culture, hRPECs inhibited hRECs in both the normal and abnormal environments.
CONCLUSION: hREC growth is inhibited by exogenous TTR under simulated DR environments with high-glucose and hypoxic, particularly in the medium containing 25 mmol/L glucose. hRPECs, which manufacture TTR in the eye, also represses hRECs in the same environment. TTR is predicted to inhibit the proliferation of hRECs and neovascularization. |
| first_indexed | 2024-12-10T03:53:49Z |
| format | Article |
| id | doaj.art-3d147463c53043ca9e023899c6975349 |
| institution | Directory Open Access Journal |
| issn | 2222-3959 2227-4898 |
| language | English |
| last_indexed | 2024-12-10T03:53:49Z |
| publishDate | 2016-06-01 |
| publisher | Press of International Journal of Ophthalmology (IJO PRESS) |
| record_format | Article |
| series | International Journal of Ophthalmology |
| spelling | doaj.art-3d147463c53043ca9e023899c69753492022-12-22T02:03:11ZengPress of International Journal of Ophthalmology (IJO PRESS)International Journal of Ophthalmology2222-39592227-48982016-06-019680981510.18240/ijo.2016.06.03Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditionsJun Shao0Yong Yao1Department of Ophthalmology, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi 214023, Jiangsu Province, ChinaDepartment of Ophthalmology, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi 214023, Jiangsu Province, ChinaAIM: To investigate biological effects of transthyretin (TTR) on the development of neovascularization under simulated diabetic retinopathy (DR) condition associated with high glucose and hypoxia. METHODS: Human retinal microvascular endothelial cells (hRECs) were cultured in normal and simulated DR environments with high glucose and hypoxia. The normal serum glucose concentration is approximately 5.5 mmol/L; thus, hyperglycemia was simulated with 25 mmol/L glucose, while hypoxia was induced using 200 µmol/L CoCl2. The influence of TTR on hRECs and human retinal pigment epithelial cells (hRPECs) was determined by incubating the cells with 4 μmol/L TTR in normal and abnormal media. A co-culture system was then employed to evaluate the effects of hRPECs on hRECs. RESULTS: Decreased hRECs and hRPECs were observed under abnormal conditions, including high-glucose and hypoxic media. In addition, hRECs were significantly inhibited by 4 μmol/L exogenous TTR during hyperglycemic culture. During co-culture, hRPECs inhibited hRECs in both the normal and abnormal environments. CONCLUSION: hREC growth is inhibited by exogenous TTR under simulated DR environments with high-glucose and hypoxic, particularly in the medium containing 25 mmol/L glucose. hRPECs, which manufacture TTR in the eye, also represses hRECs in the same environment. TTR is predicted to inhibit the proliferation of hRECs and neovascularization.http://www.ijo.cn/en_publish/2016/6/20160603.pdftransthyretindiabetic retinalhuman retinal microvascular endothelial cellshuman retinal pigment epithelial cellshyperglycemiahypoxiahypoxia |
| spellingShingle | Jun Shao Yong Yao Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions International Journal of Ophthalmology transthyretin diabetic retinal human retinal microvascular endothelial cells human retinal pigment epithelial cells hyperglycemia hypoxia hypoxia |
| title | Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| title_full | Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| title_fullStr | Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| title_full_unstemmed | Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| title_short | Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| title_sort | repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions |
| topic | transthyretin diabetic retinal human retinal microvascular endothelial cells human retinal pigment epithelial cells hyperglycemia hypoxia hypoxia |
| url | http://www.ijo.cn/en_publish/2016/6/20160603.pdf |
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