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Endothelial progenitor cells transfected with PDGF: cellular and molecular targets for prevention of diabetic
Bin Zhou1, Kai Hong Wu, Man-Chiu Poon
1State Key Laboratory of Experimental Hematology, National Research Center for Stem Cell Engineering and Technology, Institute of Hematology, Chinese Academy of Medical Sciences, Tianjin, and Fuwai Hospital, Beijing, China.
Abstract:
Microvascular insufficiency represents a major cause of end-organ failure among diabetics. Prevention at early stage of disease is therefore necessary and is a focus of current investigations. Progression of diabetes is complicated by endothelial cell apoptosis as well as occlusion of arteriole and capillary leading to microvascular rarefaction. This favors the formation of non-healing limb ulcers and limits the benefit of revascularization. Recent study indicated that reduction of platelet derived growth factor (PDGF) expression was indeed critical, in causing functional and morphological vascular changes, namely the dissociation of pericytes from the capillaries in muscles. Diabetic microangiopathy is a result of pericytes dissociation from reduced PDGF as well as vessel rarefaction from reduced number of endothelial progenitor cells (EPCs) and EPC dysfunction. Since blood vessels develop through the assembly of these two principal cell types--endothelial cells and pericytes/smooth muscle cells, prevention of diabetic microangiopathy requires interventions targeting at both cell types in a complementary and synergistic manner. An improved recruitment of EPCs will help repair of injured endothelium while molecular targeting with PDGF will enhance pericytes recruitment. EPCs modified with PDGF therefore hold promise as the next generation of agents for prevention of microangiopathy.
Insights
Diabetic microangiopathy, a cause of end-organ failure, involves pericyte loss and blood vessel rarefaction. Targeting both endothelial progenitor cells (EPCs) and platelet-derived growth factor (PDGF) offers a promising prevention strategy.
Area of Science:
- Cardiovascular Biology
- Diabetic Complications Research
- Vascular Cell Biology
Background:
- Microvascular insufficiency is a primary driver of end-organ damage in diabetes.
- Diabetes progression leads to endothelial cell apoptosis and microvascular rarefaction, causing non-healing ulcers.
- Reduced platelet-derived growth factor (PDGF) expression is linked to pericyte dissociation and vascular changes.
Purpose of the Study:
- To investigate the mechanisms of diabetic microangiopathy.
- To identify novel therapeutic targets for preventing diabetic microvascular complications.
- To explore the synergistic potential of endothelial progenitor cells (EPCs) and PDGF in vascular repair.
Main Methods:
- Analysis of cellular mechanisms in diabetic microangiopathy, focusing on pericyte and endothelial cell behavior.
- Investigating the role of PDGF in pericyte-endothelial cell interactions.
- Evaluating the therapeutic potential of modified EPCs for vascular regeneration.
Main Results:
- Diabetic microangiopathy results from pericyte dissociation (due to reduced PDGF) and vessel rarefaction (due to EPC dysfunction and reduced numbers).
- Blood vessel formation relies on both endothelial cells and pericytes/smooth muscle cells.
- Targeting both cell types offers a complementary and synergistic approach to prevention.
Conclusions:
- Preventing diabetic microangiopathy necessitates interventions addressing both endothelial progenitor cells (EPCs) and pericytes.
- Enhanced EPC recruitment can repair injured endothelium, while PDGF targeting improves pericyte recruitment.
- PDGF-modified EPCs represent a promising next-generation therapeutic for microangiopathy prevention.
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