Effects of peripheral blood monocytes on human vascular cell proliferation

doi:10.1016/0021-9150(81)90056-3

Atherosclerosis

Volume 38, Issues 3–4, February–March 1981, Pages 401-410

https://doi.org/10.1016/0021-9150(81)90056-3 Get rights and content

Abstract

Incubated human peripheral blood monocytes release a factor(s) which specifically stimulates homologous vascular smooth muscle (SMC) but not endothelial cells (EC) to proliferate in vitro.

Conditioned medium from activated monocytes significantly (P < 0.001) stimulated proliferation of SMC within 6 days of culture while media from non-activated monocytes was less effective (P < 0.01). Non-vascular smooth muscle cells (human myometrium) were less responsive to such media (P < 0.01 and P < 0.05, respectively).

These findings suggest that blood monocytes may play a key and until now unsuspected role in arterial smooth muscle cell proliferation, a recognized event in the initial stages of atherogenesis.

References (39)

E.Z. Hirsch et al.
Selective arterial endothelial injury and repair, Part 1 (Methodology and surface characteristics)
Atherosclerosis
(1977)
I.O. Ihnatowycz et al.
The effect of a platelet-derived growth factor on the proliferation of rabbit arterial smooth muscle cells in tissue culture
Thromb. Res.
(1979)
R. Ross et al.
The platelet-derived growth factor
Cell
(1978)
H.N. Antoniades et al.
Purification of human platelet-derived growth factor
N.S. Moss et al.
Human atherosclerotic plaque cells and leiomyoma cells — Comparison of in vitro characteristics
Amer. J. Path.
(1975)
A.L. Robertson
Section II. The pathogenesis of human atherosclerosis
A.L. Robertson et al.
Selective endothelial injury and repair
A.L. Robertson
Arterial endothelium in the initial stages of atherogenesis
H.R. Baumgartner et al.
Smooth muscle cell proliferation and migration after removal of arterial endothelium in rabbits
J.R. Guyton et al.
Smooth muscle cell proliferation in the occluded rat carotid artery — Lack of requirement for luminal platelets
Amer. J. Path.
(1979)

N.B. Ratliffe et al.

Platelet-leukocyte interactions following arterial endothelial injury

Amer. J. Path.

(1979)

L.K. Trejdosiewicz et al.

Growth enhancing property of human monocytes from normal donors and cancer patients

Immunology

(1979)

F. Delustro et al.

Human blood monocyte activation of human foreskin fibroblasts in vitro

S.J. Leibovich et al.

The role of the macrophage in wound repair

Amer. J. Path.

(1975)

S.J. Leibovich et al.

A macrophage-dependent factor that stimulates the proliferation of fibroblasts in vitro

Amer. J. Path.

(1976)

E.R. Unanue et al.

Synthesis and secretion of a mitogenic protein by macrophages — Description of a superinduction phenomena

J. Immunol.

(1977)

R.T. Wall et al.

Factors influencing endothelial cell proliferation in vitro

J. Cell Physiol.

(1978)

G.B. Greenburg et al.

The proliferative response in vitro of vascular endothelial and smooth muscle cells exposed to wound fluids and macrophages

J. Cell Physiol.

(1978)

R. Goldman et al.

Dual effect of normal and stimulated macrophages and their conditioned media on target cell proliferation

J. Natl. Cancer Inst.

(1979)

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^☆: These studies were supported by Grant HL-20924 of the National Institutes of Health.

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Research paperEffects of peripheral blood monocytes on human vascular cell proliferation☆

Abstract

Atherosclerosis

Thromb. Res.

Cell

Amer. J. Path.

Section II. The pathogenesis of human atherosclerosis

Selective endothelial injury and repair

Arterial endothelium in the initial stages of atherogenesis

Smooth muscle cell proliferation and migration after removal of arterial endothelium in rabbits

Smooth muscle cell proliferation in the occluded rat carotid artery — Lack of requirement for luminal platelets

Amer. J. Path.

Platelet-leukocyte interactions following arterial endothelial injury

Amer. J. Path.

Growth enhancing property of human monocytes from normal donors and cancer patients

Immunology

Human blood monocyte activation of human foreskin fibroblasts in vitro

The role of the macrophage in wound repair

Amer. J. Path.

A macrophage-dependent factor that stimulates the proliferation of fibroblasts in vitro

Amer. J. Path.

Synthesis and secretion of a mitogenic protein by macrophages — Description of a superinduction phenomena

J. Immunol.

Factors influencing endothelial cell proliferation in vitro

J. Cell Physiol.

The proliferative response in vitro of vascular endothelial and smooth muscle cells exposed to wound fluids and macrophages

J. Cell Physiol.

Dual effect of normal and stimulated macrophages and their conditioned media on target cell proliferation

J. Natl. Cancer Inst.

Research paper
Effects of peripheral blood monocytes on human vascular cell proliferation☆