endothelial progenitor cells

Endothelial damage ultimately represents a balance between the magnitude of injury and the capacity for repair.Cardiovascular risk factors induce endothelial injury and that impaired endothelial function reflects this ongoing injury.

Endothelial progenitor cells(EPC) can be isolated from circulating mononuclear cells, bone marrow, and cord blood, and might contribute to ongoing endothelial repair. They may provide a circulating pool of cells that could form a cellular patch at the site of denuding injury or serve as a cellular reservoir to replace dysfunctional endothelium.

EPC also contributes to angiogenesis-mediated tumor growth.

Circulating Endothelial Progenitor Cells, Vascular Function, and Cardiovascular Risk

N Engl J Med 2003

Using the transcription factor inhibitor of DNA binding 1 to selectively target endothelial progenitor cells offers novel strategies to inhibit tumor angiogenesis and growth.

Cancer Res  2010 

ACE inhibitors and endothelial function

ACE inhibitors block the generation of angiotensin II and prevent the breakdown of bradykinin.

Bradykinin, a potent endothelium-dependent vasodilator, causes contraction of non-vascular smooth muscle, increases vascular permeability and also is involved in the mechanism of pain. It works on the blood vessels through the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor.

ACE inhibitors improve endothelial dysfunction in patients with coronary disease and have been shown to stimulate angiogenesis and collateral vessel formation in a rabbit ischemic hindlimb model.

Tissue inhibition of angiotensin-converting enzyme activity stimulates angiogenesis in vivo.

Circulation 1999

statins and reendothelialization

Low-dose statin therapy may promote angiogenesis via multiple mechanisms, including enhanced NO production, augmented VEGF release, and activation of the Akt signaling pathway. In addition, statins also increase endothelial progenitor cell (EPC) mobilization and accelerate reendothelialization after vascular injury.

Statin Therapy Accelerates Reendothelialization 

Circulation 2002

regulation of angiogenesis

In response to stimuli such as hypoxia, VEGF induces vasculogenesis and endothelial cell proliferation. Ang1–Tie2 interactions mediate vessel maturation and maintain vessel integrity through the recruitment of peri-endothelial cells. Ang2 blocks Ang1–Tie2 signaling, loosening vascular structure and exposing the endothelium to inducers of angiogenesis such as VEGF. In the presence of VEGF, endothelial cells migrate and proliferate to form new capillary sprouts and blood vessels. Ang2 expression in the absence of VEGF stimulation leads to vessel regression and apoptosis. RTK indicates receptor tyrosine kinase.

Clinician Guide to Angiogenesis

Circulation 2003

endothelium covering atherosclerotic plaque

Scanning ME of the surface of endothelium covering atherosclerotic plaque (magnification x2400). Endothelial cells contains numerous microvilli (indicated by arrows). Agreggated platetels and leukocytes adhering to endothelium are visible.

Ultrastructural Alteration of Endothelium Covering Advanced Atherosclerotic Plaque in Human Carotid Artery Visualized by Scanning Electrom Microscope

macrophages on endothelium

http://www.mc.vanderbilt.edu/research-em/REMC%20Files/Image_Gallery.htm