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(Circulation Research. 2008;102:507.)
© 2008 American Heart Association, Inc.

Editorials

A Vascular Bone Collector

Arterial Calcification Requires Tissue-Type Transglutaminase

Ed VanBavel, Erik N.T.P. Bakker

From the Department of Medical Physics, Academic Medical Center, The Netherlands.

Correspondence to Ed VanBavel, Department of Medical Physics, Academic Medical Center, The Netherlands, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail E.vanbavel@amc.uva.nl

See related article, pages 529–537

Key Words: transglutaminase • atherosclerosis • smooth muscle cell • calcification

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

Calcification of the arterial wall occurs in, among others, atherosclerosis and aging. The role of calcification in plaque stability is subject of ongoing discussion; media calcification in aging and diabetes increases stiffness and pulse pressure.¹ It is now clear that calcification is not simply a passive process but, rather, is tightly regulated, involving induction of an osteochondrogenic phenotype in the vascular smooth muscle cells (VSMCs) and control of expression and activity of factors promoting and inhibiting calcium deposition. In this issue of Circulation Research, Johnson et al² provide evidence that transglutaminases (Tgases), cross-linking enzymes with recently discovered vascular functions, are required for inducing the vascular calcification process.

Tgases are multifunctional enzymes acting in the cell, at the cell surface, or as released enzymes. Their most prominent feature is the covalent cross-linking of proteins.³ The glutamine–lysine cross-links, either within or between proteins, result in the stabilization of extracellular matrices and the binding of signaling molecules, such as osteopontin, to the matrix but also the prolonged activation of angiotensin II receptors through dimerization.⁴ Cell surface Tgases are involved in cell adhesion through integrin clustering and function as coreceptors in the binding to fibronectin.⁵ The Tgase family consists of 9 members, of which TG1, TG2, and the coagulation factor XIIIA are expressed in the arterial wall.⁶ The tissue-type Tgase studied here (TG2) fulfills both cross-linking activities and G protein functions. Mice deficient in TG2 have no obvious cardiovascular phenotype. However, when challenged, arteries show impaired capacity to undergo inward remodeling in response . . . [Full Text of this Article]

Related Article:

Transglutaminase 2 Is Central to Induction of the Arterial Calcification Program by Smooth Muscle Cells

Kristen A. Johnson, Monika Polewski, and Robert A. Terkeltaub
Circ. Res. 2008 102: 529-537. [Abstract] [Full Text] [PDF]