Role of pericytes in vascular calcification: a review

Abstract

Pericytes are defined by their location in vivo; the pericyte partially surrounds the endothelial cell of the microvessel and shares a common basement membrane with it. As an integral part of the microvasculature, pericytes play a fundamental role in maintaining local and tissue homeostasis. Current evidence also suggests that pericytes function as progenitor cells capable of differentiating into a variety of different cell types including osteoblasts, chondrocytes and adipocytes. It is now apparent that cells resembling microvascular pericytes, and termed 'pericyte-like' cells, have a widespread distribution in vivo. Pericyte-like cells have been identified in the inner intima, the outer media, and in the vasa vasora of the adventitia of large, medium and small human arteries (1, 2). Moreover, recent studies have suggested that these cells may be responsible, at least in part, for mediating the calcification commonly associated with atherosclerosis (1, 3, 4). In this review, we a) examine the evidence that microvascular pericytes deposit a bone-like mineralised matrix in vitro, b) compare the morphological and biochemical properties of microvascular pericytes, calcifying vascular cells (CVCs) and 'classical' smooth muscle cells (SMCs) isolated from bovine aorta, c) demonstrate that microvascular pericytes deposit a well-organised matrix of bone, cartilage and fibrous tissue in vivo, and d) discuss recent studies designed to gain a better understanding of how pericyte differentiation is regulated.

Culture medium modulates the behaviour of human dental pulp-derived cells: Technical Note

“…This data therefore appears in agreement with previous reports, which showed that MEM could be successfully employed in culture of cells expressing smooth muscle cell markers (pericytes or calcifying vascular cells). Indeed, these cells routinely cultured in MEM spontaneously formed multicellular nodules that mineralized without exogenous factors (Schor et al, 1995;Proudfoot et al, 1998;Canfield et al, 2000). However, in order to explain the lower proportion of SMA+ cells in RPMI 1640 medium, we can hypothesize that the high phosphate concentration (5mM) had induced a phenotypic transition characterized by a loss of α-smooth muscle actin as previously described in bovine aortic smooth muscle cells (Steitz et al, 2001).…”

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

“…Cellular transformation to a myofibroblastic phenotype commonly occurs during wound healing and tissue injury (32). Pericytes have been indicated to function as progenitor cells capable of differentiating into a variety of cell types and synthesizing collagen during inflammation, injury repair, or angiogenesis (6,11). In particular, PAF, normally released by activated leukocytes and endothelial cells during inflammation, has been reported to be able to act as a direct cytokine and stimulate lung pericyte growth in vitro (24).…”

Chondrogenic and Adipogenic Potential of Microvascular Pericytes

“…Finally, pericytes may be involved in the development and progression of several pathological conditions, including vascular calcification. 30,31 Indeed, markers of both cartilage and bone have been identified in calcified blood vessels, [31][32][33][34][35] and it has been suggested that a subpopulation of SM cells that resemble pericytes (calcifying vascular cells) contributes to this calcification. 30 -32 A recent study has shown that these cells also have multilineage potential in vitro.…”