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(Circulation Research. 2009;104:1038.)
© 2009 American Heart Association, Inc.

Editorials

Vascular Progenitor Cells in Diabetes Mellitus

Roles of Wnt Signaling and Negatively Charged Low-Density Lipoprotein

Chu-Huang Chen, Richard A.F. Dixon, Liang-Yin Ke, James T. Willerson

From the Department of Medicine, Baylor College of Medicine (C.-H.C., L.-Y.K.), Houston, Tex; Texas Heart Institute (R.A.F.D., J.T.W.), Houston; China Medical University Hospital (C.-H.C.), Taichung, Taiwan; and Kaohsiung Medical University Hospital (L.-Y.K.), Kaohsiung, Taiwan.

Correspondence to Chu-Huang Chen, MD, PhD, Baylor College of Medicine, 6565 Fannin St, MS A-601, Houston, TX 77030. E-mail cchen@bcm.tmc.edu

See related article, pages 1095–1102

Key Words: CD133 • Wnt • diabetes • L5 • microRNA

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Over the centuries, diabetes mellitus–associated ischemic ulcers have driven physicians to continue to improve their skills in healing the ulcers to prevent devastating complications.¹ Unfortunately, extremity amputation still remains the outcome in many cases. The recent development of vascular progenitor cell (PC) transplantation aimed at enhancing angiogenesis and wound healing may, however, provide new hope in the treatment of this old ailment.^2,3 In this issue of Circulation Research, Barcelos et al show in a murine diabetes mellitus model that topical transplantation of human fetal CD133⁺ PCs significantly accelerates the healing of skin wounds on ischemic hind limbs.⁴ Their data suggest that the reparative angiogenesis is mediated by the wingless (Wnt) signaling pathway.

The prominin-1 (PROM1)/CD133 gene encodes a pentaspan transmembrane glycoprotein expressed in a variety of stem cells, including hematopoietic stem cells, endothelial PCs (EPCs), and neuronal/glial stem cells.^5,6 By suppressing further differentiation, PROM1 helps these cells maintain their stem cell properties. Mutations in PROM1 may result in retinitis pigmentosa,⁷ and its overexpression is also associated with cancer formation.⁸ In view of this cancer potential, overstimulation of CD133⁺ cells may also lead to unwanted consequences. Additionally, that human fetal CD133⁺ cells are not easily accessible makes this approach clinically impractical. Of importance, however, the gist of the work by Barcelos et al⁴ is not in promoting the use of human fetal CD133⁺ cells in common practice but, rather, in the enhancement of Wnt-dependent signaling in local endothelial cells (ECs) induced by PROM1/CD133 through a paracrine mechanism. This is supported . . . [Full Text of this Article]

Related Article:

Human CD133⁺ Progenitor Cells Promote the Healing of Diabetic Ischemic Ulcers by Paracrine Stimulation of Angiogenesis and Activation of Wnt Signaling

Lucíola S. Barcelos, Cécile Duplaa, Nicolle Kränkel, Gallia Graiani, Gloria Invernici, Rajesh Katare, Mauro Siragusa, Marco Meloni, Ilaria Campesi, Manuela Monica, Andreas Simm, Paola Campagnolo, Giuseppe Mangialardi, Lara Stevanato, Giulio Alessandri, Costanza Emanueli, and Paolo Madeddu
Circ. Res. 2009 104: 1095-1102. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				R. Ascione and P. Madeddu Risk and Benefit of CD133+ Progenitors Circ. Res., July 17, 2009; 105(2): e2 - e2. [Full Text] [PDF]