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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1707.)
© 2003 American Heart Association, Inc.

Editorials

Regulating Cross-Talk Between Vascular Smooth Muscle Cells

Thomas N. Tulenko

From the Departments of Surgery, Biochemistry, and Molecular Pharmacology, Thomas Jefferson University College of Medicine, Philadelphia, Pa.

Correspondence to Thomas N. Tulenko, PhD, Professor, Department of Surgery, Thomas Jefferson University School of Medicine, 1025 Walnut St, Ste 605, Philadelphia, PA 19107. E-mail thomas.tulenko@jefferson.edu

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

Gap junctions are small pore-forming protein connections between neighboring cells that mediate the flow of ions and small molecules (1 200 Da). As such, they provide a degree of direct cytoplasmic continuity between cells that contributes, along with paracrine pathways, to the intercellular flow of information. These channels are often thought to be long-lived, nonspecific conduits allowing the cell-to-cell spread of ionic currents and small signaling molecules such as cAMP, cGMP, etc. However, in recent years, new evidence has dramatically improved our appreciation of their diversity, regulation, and contribution to normal tissue function and, importantly, has advanced our understanding of the pathogenesis of various diseases. For example, in oncology, the growth and spread of malignant cells in a variety of cancers appears to be dependent on establishing gap junction connections between normal and malignant cells.^1,2 In cardiovascular medicine, gap junction alterations have been implicated in the genesis of cardiac arrhythmias,³ remodeling of the arterial wall in hypertension,^4–6 and perhaps atherosclerosis.^7–9 Indeed, the list goes on, including pathologies in the ophthalmic, neurologic, gastrointestinal, and endocrine systems. Considering their involvement in tissue physiology and pathophysiology, it is essential that we move forward in unraveling the regulatory mechanisms underlying gap junction protein expression and function. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Cowan and his colleagues¹⁰ in Toronto and Boston describe an elegant series of experiments demonstrating that the principle gap junction protein in vascular smooth muscle cells, Cx43, is transcriptionally upregulated by hypoxia and stretch, which surprisingly appears . . . [Full Text of this Article]