Published online Oct 26, 2020. doi: 10.4252/wjsc.v12.i10.1152
Peer-review started: May 15, 2020
First decision: June 7, 2020
Revised: June 18, 2020
Accepted: August 25, 2020
Article in press: August 25, 2020
Published online: October 26, 2020
Processing time: 163 Days and 18.5 Hours
The loss of pericytes, which occurs in diabetic retinopathy, results in a breakdown of the blood-retina barrier (BRB) and infiltration of inflammatory cells. Lost retinal pericytes might be replaced by adipose-derived mesenchymal stem cells (ASCs) after differentiating into a pericyte-like phenotype.
The use of pericyte-like differentiated ASCs may represent a valuable therapeutic strategy for restoring BRB damage.
The purpose of this study was to develop in vitro strategies to obtain pericyte-like differentiation of human ASCs.
Different ASC culture conditions were tested and compared to human retinal pericytes (hRPCs). The expression of α-smooth muscle actin (α-SMA) and neural/glial antigen 2 (NG2) was assessed by immunocytochemical staining and western blotting. In co-cultures of human retinal endothelial cells (hRECs) with hRPCs or different groups of hASCs, the endothelial expression of typical junctional proteins such as vascular endothelial-Cadherin, zonula occludens-1 and Occludin were evaluated. In an in vitro model of BRB, the trans-endothelial electrical resistance was measured. Three-dimensional co-cultures in Matrigel of hRECs and hRPCs or pericyte-like hASCs were designed to assess their reciprocal localization.
Immunocytochemical results and western blot analysis for α-SMA and NG2 indicated that the closest pericyte-like phenotype was observed when hASCs were cultured in pericyte medium (PM-hASCs). α-SMA immunoreactivity was strongly increased only when TGF was added to the culture medium. NG2 expression, almost undetectable in most conditions, was substantially increased in PM-hASCs.
In co-culture experiments, immunoreactivity of vascular endothelia-Cadherin, zonula occludens-1 and Occludin was considerably increased in hRECs when hRPCs or PM-hASCs were also present. Supporting results were found by trans-endothelial electrical resistance measurements, showing the highest values in analogous conditions. The pericyte-like phenotype of PM-hASCs was also confirmed in three-dimensional co-cultures in Matrigel, where PM-hASCs and hRPCs similarly localized around the tubular formations made by hRECs.
PM-hASCs seem able to strengthen the intercellular junctions between hRECs, likely reinforcing the BRB; thus, hASC-based therapeutic approaches may be usefully developed to restore the integrity of retinal microcirculation.
Future in vivo experiments will be designed to test pericyte-like ASC engraftment following intraocular administration. Possible beneficial effects will be evaluated in animal models of diabetic retinopathy. Eventually, when safe therapeutic protocols are developed, ASC-based therapeutic approaches may be successfully used in diabetic patients to restore disrupted retinal microcirculation.