Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation
Diabetic retinopathy is considered a neurovascular disorder, hyperglycemia being considered the main risk factor for this pathology. Diabetic retinopathy also presents features of a low-grade chronic inflammatory disease, including increased levels of cytokines in the retina, such as interleukin-1 b...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2017-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/4316316 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832561834349035520 |
|---|---|
| author | Filipa I. Baptista Célia A. Aveleira Áurea F. Castilho António F. Ambrósio |
| author_facet | Filipa I. Baptista Célia A. Aveleira Áurea F. Castilho António F. Ambrósio |
| author_sort | Filipa I. Baptista |
| collection | DOAJ |
| description | Diabetic retinopathy is considered a neurovascular disorder, hyperglycemia being considered the main risk factor for this pathology. Diabetic retinopathy also presents features of a low-grade chronic inflammatory disease, including increased levels of cytokines in the retina, such as interleukin-1 beta (IL-1β). However, how high glucose and IL-1β affect the different retinal cell types remains to be clarified. In retinal neural cell cultures, we found that IL-1β and IL-1RI are present in microglia, macroglia, and neurons. Exposure of retinal neural cell cultures to high glucose upregulated both mRNA and protein levels of IL-1β. High glucose decreased microglial and macroglial cell proliferation, whereas IL-1β increased their proliferation. Interestingly, under high glucose condition, although the number of microglial cells decreased, they showed a less ramified morphology, suggesting a more activated state, as supported by the upregulation of the levels of ED-1, a marker of microglia activation. In conclusion, IL-1β might play a key role in diabetic retinopathy, affecting microglial and macroglial cells and ultimately contributing to neural changes observed in diabetic patients. Particularly, since IL-1β has an important role in retinal microglia activation and proliferation under diabetes, limiting IL-1β-triggered inflammatory processes may provide a new therapeutic strategy to prevent the progression of diabetic retinopathy. |
| format | Article |
| id | doaj-art-4e0b20c5cb69425798ba261241d0ff27 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4e0b20c5cb69425798ba261241d0ff272025-02-03T01:24:00ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/43163164316316Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell ProliferationFilipa I. Baptista0Célia A. Aveleira1Áurea F. Castilho2António F. Ambrósio3Institute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Coimbra, PortugalCenter for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, PortugalInstitute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Coimbra, PortugalInstitute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Coimbra, PortugalDiabetic retinopathy is considered a neurovascular disorder, hyperglycemia being considered the main risk factor for this pathology. Diabetic retinopathy also presents features of a low-grade chronic inflammatory disease, including increased levels of cytokines in the retina, such as interleukin-1 beta (IL-1β). However, how high glucose and IL-1β affect the different retinal cell types remains to be clarified. In retinal neural cell cultures, we found that IL-1β and IL-1RI are present in microglia, macroglia, and neurons. Exposure of retinal neural cell cultures to high glucose upregulated both mRNA and protein levels of IL-1β. High glucose decreased microglial and macroglial cell proliferation, whereas IL-1β increased their proliferation. Interestingly, under high glucose condition, although the number of microglial cells decreased, they showed a less ramified morphology, suggesting a more activated state, as supported by the upregulation of the levels of ED-1, a marker of microglia activation. In conclusion, IL-1β might play a key role in diabetic retinopathy, affecting microglial and macroglial cells and ultimately contributing to neural changes observed in diabetic patients. Particularly, since IL-1β has an important role in retinal microglia activation and proliferation under diabetes, limiting IL-1β-triggered inflammatory processes may provide a new therapeutic strategy to prevent the progression of diabetic retinopathy.http://dx.doi.org/10.1155/2017/4316316 |
| spellingShingle | Filipa I. Baptista Célia A. Aveleira Áurea F. Castilho António F. Ambrósio Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation Mediators of Inflammation |
| title | Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation |
| title_full | Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation |
| title_fullStr | Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation |
| title_full_unstemmed | Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation |
| title_short | Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation |
| title_sort | elevated glucose and interleukin 1β differentially affect retinal microglial cell proliferation |
| url | http://dx.doi.org/10.1155/2017/4316316 |
| work_keys_str_mv | AT filipaibaptista elevatedglucoseandinterleukin1bdifferentiallyaffectretinalmicroglialcellproliferation AT celiaaaveleira elevatedglucoseandinterleukin1bdifferentiallyaffectretinalmicroglialcellproliferation AT aureafcastilho elevatedglucoseandinterleukin1bdifferentiallyaffectretinalmicroglialcellproliferation AT antoniofambrosio elevatedglucoseandinterleukin1bdifferentiallyaffectretinalmicroglialcellproliferation |