α5β1 Integrin Expression and Luminal Edge Fibronectin Matrix Assembly by Smooth Muscle Cells after Arterial Injury

Pickering, J. Geoffrey; Chow, Lawrence H.; Li, Shaohua; Rogers, Kem A.; Rocnik, Edward; Zhong, Robert; Chan, Bosco M.C.

doi:10.1016/s0002-9440(10)64750-5

Cited by 80 publications

(67 citation statements)

References 38 publications

(42 reference statements)

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“…24 Cells fixed with 4% paraformaldehyde were immunostained for SM ␣-actin, h-caldesmon (hHCD, Sigma), and factor VIII-related antigen (F8/86, DAKO), as described previously. 4 …”

Section: Western Blot Analysis and Immunostainingmentioning

confidence: 99%

“…This is most apparent in diseased or injured arteries where SMCs within the intima can be distinguished from those in the underlying media based on morphology 1 and differential expression of contractile apparatus proteins, 2,3 integrins, 4 extracellular matrix molecules, [5][6][7] and growth factors. 8,9 Typically, the differences suggest the presence of relatively less specialized SMCs within the remodeling arterial intima, which is in accordance with their role in expanding and restructuring the vessel wall.…”

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confidence: 99%

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Innate Diversity of Adult Human Arterial Smooth Muscle Cells

Fan

Chow

et al. 2001

Circulation Research

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125

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Abstract-Vascular smooth muscle cells (SMCs) perform diverse functions and this functional heterogeneity could be based on differential recruitment of distinct SMC subsets. In humans, however, there is little support for such a paradigm, partly because isolation of pure human SMC subsets has proven difficult. We report the cloning of 12 SMC lines from a single fragment of human internal thoracic artery and the elucidation of 2 distinct cellular profiles. Epithelioid clones (nϭ9) were polygonal at confluence, 105Ϯ9 m in length, and had a doubling time of 39Ϯ2 hours. Spindle-shaped clones (nϭ3) were larger (267Ϯ18 m long, PϽ0.01) and grew slower (doubling time 65Ϯ4 hours, PϽ0.01). Both types of clones expressed smooth muscle (SM) ␣-actin, SM-myosin heavy chains, h-caldesmon, and calponin, but only spindle-shaped clones expressed metavinculin. Epithelioid clones displayed greater proliferation in response to platelet-derived growth factor-BB and fibroblast growth factor-2 and were more responsive to the migratory effect of platelet-derived growth factor-BB. Spindle-shaped clones showed more robust Ca 2ϩ transients in response to angiotensin II, histamine, and norepinephrine, crawled more quickly, and expressed more type I collagen. On serum withdrawal, spindle-shaped clones differentiated into a contraction-competent cell. A regional basis for diversity among SMCs was suggested by stepwise arterial digestion, which liberated small, SM ␣-actin-positive cells from the abluminal medial layers and larger SMCs from all layers. These results identify inherent SMC diversity in the media of the adult internal thoracic artery and suggest differential participation of SMC subsets in the regulation of human arterial behavior. (Circ Res. 2001;89:517-525.)

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“…24 Cells fixed with 4% paraformaldehyde were immunostained for SM ␣-actin, h-caldesmon (hHCD, Sigma), and factor VIII-related antigen (F8/86, DAKO), as described previously. 4 …”

Section: Western Blot Analysis and Immunostainingmentioning

confidence: 99%

mentioning

confidence: 99%

Innate Diversity of Adult Human Arterial Smooth Muscle Cells

Fan

Chow

et al. 2001

Circulation Research

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125

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“…12 In the present study, we tested the hypothesis that outgrowth from human peripheral blood MNC in PDGF BB-enriched medium would result in SPC differentiation into smooth muscle outgrowth cells (SOCs). Furthermore, because ␤ 1 integrins are considered to play a major role in homing of blood-borne progenitor cells 12 and are essential for vascular smooth muscle adhesion, matrix assembly, and cell proliferation, 13,14 we also hypothesized that the integrin ␣ 5 ␤ 1 (the most highly abundant ␤ 1 integrin in proliferating smooth muscle cells in vivo) 15 would be important in SOC adhesion.…”

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confidence: 99%

Smooth Muscle Progenitor Cells in Human Blood

et al. 2002

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Background-Recent animal data suggest that vascular smooth muscle cells within the neointima of the vessel wall may originate from bone marrow, providing indirect evidence for circulating smooth muscle progenitor cells (SPCs). Evidence for circulating SPCs in human subjects does not exist, and the mechanism whereby such putative SPCs may home to sites of plaque formation is presently not understood but is likely to involve expression of specific surface adhesion molecules, such as integrins. In this study, we aimed to culture smooth muscle outgrowth cells (SOCs) from SPCs in human peripheral blood and characterize surface integrin expression on these cells. Methods and Results-Human mononuclear cells isolated from buffy coat were seeded on collagen type 1 matrix and outgrowth cells selected in endothelial growth medium (EGM-2) or EGM-2 and platelet-derived growth factor BB. Selection in platelet-derived growth factor BB-enriched medium caused rapid outgrowth and expansion of SOC to Ͼ40 population doublings in a 4-month period. These SOCs were positive for smooth muscle cell-specific ␣ actin (␣SMA), myosin heavy chain, and calponin on immunofluorescence and Western blotting and were also positive for CD34, Flt1, and Flk1 receptor but negative for Tie-2 receptor expression, suggesting a potential bone marrow angioblastic origin. In contrast, endothelial outgrowth cells (EOCs) grown in EGM-2 alone and the initial MNC population were negative for these smooth muscle-specific markers. Integrin ␣ 5 ␤ 1 expression by FACS and Western blotting was significantly increased in SOCs compared with EOCs, and this was confirmed by 8-fold greater adhesion of SOC to fibronectin (PϽ0.001), an effect that could be decreased using an ␣ 5 ␤ 1 antibody. Finally, SOC showed a significantly greater in vitro proliferative potential compared with EOCs of similar passage (PϽ0.001). Conclusions-This study demonstrates for the first time outgrowth of smooth muscle cells with a specific growth, adhesion, and integrin profile from putative SPC in human blood. These data have implications for our understanding of adult vascular smooth muscle cell differentiation, proliferation, and homing.

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“…Some of the integrins that are poorly expressed in contractile VSMCs, especially a2b1, a5b1 and avb3, become more prominent in non-contractile state 33 and mediate VSMC migration. [34][35][36][37] a2b1 integrin, a collagen receptor, has been implicated in platelet-derived growth factor (PDGF)-induced VSMC migration. 34 It has been reported that stress fiber disassembly by fibroblast growth factor may promote the differential utilization of a2b1 integrin for VSMC motility.…”

Section: Integrin or Integrins?mentioning

confidence: 99%

“…However, they are upregulated in phenotype-modulated VSMCs and promote migration. 35,36 avb3 is one of the most-studied integrins. avb3 and avb5 integrins both mediate VSMC migration.…”

Section: Integrin or Integrins?mentioning

confidence: 99%

Tensegrin in context

Zargham

2010

Cell Adhesion & Migration

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α5β1 Integrin Expression and Luminal Edge Fibronectin Matrix Assembly by Smooth Muscle Cells after Arterial Injury

Cited by 80 publications

References 38 publications

Innate Diversity of Adult Human Arterial Smooth Muscle Cells

Innate Diversity of Adult Human Arterial Smooth Muscle Cells

Smooth Muscle Progenitor Cells in Human Blood

Tensegrin in context

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