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(Circulation Research. 2003;93:1139.)
© 2003 American Heart Association, Inc.

Editorials

All Strain, No Gain

Stretch Keeps Proliferation at Bay via the NF-B Response Gene iex-1

Stéphanie Lehoux, Alain Tedgui

From INSERM U541 and Institut Fédératif de Recherche–Paris-7, Hôpital Lariboisière, Paris, France.

Correspondence to Alain Tedgui, PhD, INSERM U541, 41, Bd de la Chapelle, 75010 Paris, France. E-mail tedgui@larib.inserm.fr

Key Words: mechanotransduction • stretch • smooth muscle cells • phenotype • nuclear factor-B

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

Blood vessels are continuously subjected to the action of mechanical forces in the form of shear stress and tensile stress. Shear stress results from the friction of blood against the vessel and is sensed by endothelial cells. Tensile stress is the product of blood pressure, and it is the major determinant of vessel stretch, to which a cyclic quality is added stemming from the pulsatile nature of blood pressure. Stretch affects both endothelial cells and smooth muscle cells (SMCs).

Alterations in the biomechanical environment induce transformations in the vessel wall to accommodate any new hemodynamic conditions and ultimately restore basal levels of tensile stress and shear stress.¹ In vivo studies and clinical observations suggest that decreased values of tensile and shear stress are correlated with enhanced cell proliferation and extracellular matrix production, whereas reestablishment of baseline tensile stress and shear stress levels is associated with restoration of vessel wall morphology and a return of SMCs to a differentiated state.² In fact, a distinct feature of vascular SMCs is their phenotypic plasticity: SMCs are capable of displaying broad changes in ultrastructure and marker protein expression depending on their environment.³ This feature is particularly evident in SMCs undergoing a transition from the contractile to the synthetic phenotype such as occurs during establishment of primary cell cultures or at the loci of vascular injury.³ For example, nonmuscle ß-actin mRNA and protein levels markedly increase in SMCs placed in culture.⁴ Interestingly, mechanical factors play a major role in determining SMC phenotype. Exposing cultured SMCs . . . [Full Text of this Article]

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