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Figure 8

ID: ZDB-IMAGE-210817-27
Publication: Sehgal et al., 2021 - LncRNA VEAL2 regulates PRKCB2 to modulate endothelial permeability in diabetic retinopathy
All Figures: Figures for Sehgal et al., 2021

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Figure Caption

Figure 8 PRKCB‐<italic toggle='yes'>VEAL2</italic> interplay in maintenance of basal endothelial permeability

Hypothetical schema showing normal endothelial cell (left), in which the apparent competitive binding of DAG and VEAL2 to the C1 domain of PRKCB restricts the activation of PRKCB and phosphorylation of junctional proteins. The controlled turnover of junctional proteins dictates the basal endothelial permeability and maintains homeostasis. Under hyperglycemic conditions (right), excessive glucose increases DAG levels in endothelial cells. Increased DAG levels further outcompete VEAL2 and hyperactivate PRKCB, enabling increased translocation to membrane. During this condition, junctional protein turnover and degradation is unchecked and leads to hyperpermeability. VEGF‐vascular endothelial growth factor, VEGFR2‐vascular endothelial growth factor receptor 2, PLCγ‐phospholipase C gamma, PIP2‐phosphatidylinositol‐4,5‐bisphosphate, DAG‐diacylglycerol, PRKCB‐protein kinase C beta, and VEAL2‐vascular endothelial‐associated lncRNA 2.

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