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Published on: May 5, 2021
Severe hypoglycaemia-induced microglial inflammation damages microvascular endothelial cells, leading to retinal
Yuxin Hu1, Zhen Li1, Hongxue Li1
1The Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Abstract:
Human microglia (HMC) are stress-induced inflammatory cells of the retina. It is unknown whether severe hypoglycaemia causes inflammation in microglia, affects the permeability of human retinal microvascular endothelial cells (HRMECs), and causes retinal damage. This study aimed to explore the effects of severe hypoglycaemia on retinal microglial inflammation and endothelial cell permeability and evaluate the damage caused by hypoglycaemia to the retina. The CCK-8 assay was used to measure cell viability. Western blotting was used to detect IL-1β, IL-6, TNF- α, claudin-1, and occludin expression. ELISA was used to detect IL-1β, IL-6, and TNF- α. Transmission electron microscopy (TEM) and haematoxylin and eosin staining were used to observe the retinal structure. Immunohistochemistry and immunofluorescence staining assays were also used to detect IL-1β, IL-6, TNF- α, claudin-1, and occludin expression. Severe hypoglycaemia promoted inflammation in HMC3 cells. Inflammation caused by hypoglycaemia leads to the decreased expression of tight junction proteins. In vivo, severe hypoglycaemia induced structural damage to the retina, increased the expression of inflammatory factors, and decreased the expression of tight junction proteins. Our results suggest that severe hypoglycaemia leads to acute retinal inflammation, affecting the permeability of HRMECs and causing retinal damage.
Insights
Severe hypoglycemia causes retinal inflammation and damage by activating microglia and increasing blood-retinal barrier permeability. This study reveals hypoglycemia
Area of Science:
- Ophthalmology
- Neuroscience
- Cell Biology
Background:
- Human microglia (HMC) are retinal cells activated by stress.
- The impact of severe hypoglycemia on retinal microglia, endothelial cells, and overall retinal integrity remains unclear.
Purpose of the Study:
- To investigate the effects of severe hypoglycemia on retinal microglial inflammation.
- To assess changes in human retinal microvascular endothelial cell (HRMEC) permeability under hypoglycemic conditions.
- To evaluate the extent of retinal damage induced by severe hypoglycemia.
Main Methods:
- Cell viability assessed using CCK-8 assay.
- Protein expression (IL-1β, IL-6, TNF-α, claudin-1, occludin) analyzed via Western blotting, ELISA, immunohistochemistry, and immunofluorescence.
- Retinal structural changes observed using Transmission Electron Microscopy (TEM) and Hematoxylin and Eosin staining.
Main Results:
- Severe hypoglycemia significantly promoted inflammation in HMC3 cells.
- Hypoglycemia-induced inflammation led to decreased expression of tight junction proteins (claudin-1, occludin).
- In vivo, severe hypoglycemia caused retinal structural damage, elevated inflammatory factors, and reduced tight junction protein expression.
Conclusions:
- Severe hypoglycemia triggers acute retinal inflammation.
- Hypoglycemia compromises the permeability of HRMECs.
- The study demonstrates that severe hypoglycemia leads to significant retinal damage.
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