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(Circulation Research. 2005;97:4.)
© 2005 American Heart Association, Inc.

Editorials

Pre–B-cell Colony-Enhancing Factor Regulates Vascular Smooth Muscle Maturation Through a NAD⁺-Dependent Mechanism

Recognition of a New Mechanism for Cell Diversity and Redox Regulation of Vascular Tone and Remodeling

Stephen L. Archer

From the Department of Medicine (Cardiology), Department of Physiology, and the Vascular Biology Group, University of Alberta, Edmonton, Canada.

Correspondence to Dr Stephen L. Archer, Heart and Stroke Chair in Cardiovascular Research, Chair, Cardiology Division, Department of Medicine, University of Alberta, WMC 2C2.36, 8440 112th St, Edmonton, Alberta, Canada, T6G 2B7. E-mail sarcher@cha.ab.ca

See related article, pages 25–34

Key Words: nicotinamide phosphoribosyltranferase (NAmPRTase) • survivin • redox signaling • NAD⁺-dependent histone deacetylase • pulmonary hypertension

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

	Introduction

 
There is a growing recognition of diversity in the morphology and function of vascular smooth muscle cells (SMCs). Diversity is both visible, with SMCs of different shape coexisting in arteries, and functional, manifest through differences in ionic profile, oxygen-sensitivity, proliferative capacity, and apoptosis susceptibility. SMC diversity is evident temporally (differences within a segment during development) and geographically (differences in SMCs between functionally discrete vascular segments within a single circulation).¹ Moreover, many vibrant "vascular villages" display rich diversity within a single vascular segment, with heterogeneity in SMCs that exist side by side.^2,3

The article by Pickering’s group addresses the molecular mechanism underlying a form of SMC diversity that has morphological and functional aspects; namely the existence of synthetic versus contractile SMCs.⁴ It is an important contribution because, in addressing their own hypothesis, they reveal a mechanism that has relevance to several unresolved questions in vascular biology.⁴ How do blood vessels regulate the transition from fetus to adult? What is the molecular basis for SMC diversity? How does acute redox regulation of vascular tone translate to altered vascular structure in hypertension? By providing partial answers to these questions, their work has implications for hypoxic pulmonary vasoconstriction (HPV),^1,2 pulmonary hypertension,³ systemic hypertension, vascular repair, and atherosclerosis.

The Pickering group used 2 clonal SMC lines, derived from human mammary arteries, to study the molecular mechanism for the maturational conversion from a proliferative to a constrictive phenotype. One cell line mimicked the SMC in fetal or healing arteries, being morphologically "Rubenesque" and possessed a synthetic . . . [Full Text of this Article]

Related Article:

Pre–B-Cell Colony–Enhancing Factor Regulates NAD⁺-Dependent Protein Deacetylase Activity and Promotes Vascular Smooth Muscle Cell Maturation

Eric van der Veer, Zengxuan Nong, Caroline O’Neil, Brad Urquhart, David Freeman, and J. Geoffrey Pickering
Circ. Res. 2005 97: 25-34. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				K. R. Stenmark, K. A. Fagan, and M. G. Frid Hypoxia-Induced Pulmonary Vascular Remodeling: Cellular and Molecular Mechanisms Circ. Res., September 29, 2006; 99(7): 675 - 691. [Abstract] [Full Text] [PDF]