Human dermal microvascular endothelial cells in vitro: Effect of cyclic AMP on cellular morphology and proliferation rate

Davison, Pamela; Karasek, Marvin A.

doi:10.1002/jcp.1041060211

Cited by 88 publications

(35 citation statements)

References 9 publications

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“…In human dermal capillary cells, CT and the phosphodiesterase inhibitor isobutylmethylxanthine have been shown to stimulate cell proliferation (35).…”

Section: Discussionmentioning

confidence: 99%

Calcitonin gene-related peptide stimulates proliferation of human endothelial cells.

Hægerstrand

Dalsgaard²,

Jonzon³

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

263

118

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The effects of the vasoactive perivascular neuropeptides calcitonin gene-related peptide (CGRP), neurokinin A (NKA), neuropeptide Y (NPY), and vasoactive intestinal polypeptide (VIP) on proliferation of cultured human umbilical vein endothelial cells (HUVECs) were investigated. CGRP was shown to increase both cell number and DNA synthesis, whereas NKA, NPY, and VIP were ineffective. l I-labeled CGRP was shown to bind to HUVECs and this binding was displaced by addition of unlabeled CGRP, suggesting the existence of specific CGRP receptors. The effect of CGRP on formation of adenosine 3',5'-cycdic monophosphate (cAMP) and inositol phosphates (InsP), two intracellular messengers known to be involved in regulation of cell proliferation, was investigated. CGRP stimulated cAMP formation but was without effect on the formation of InsP. Proliferation, as well as cAMP formation, was also stimulated by cholera toxin. Basic fibroblast growth factor stimulated growth without affecting cAMP or InsP formation, whereas thrombin, which increased InsP formation, did not stimulate proliferation. We thus suggest that CGRP may act as a local factor stimulating proliferation of endothelial cells; that the mechanism of action is associated with cAMP formation; and that this effect of CGRP may be important for formation of new vessels during physiological and pathophysiological events such as ischemia, inflammation, and wound healing. Several different factors have been shown to stimulate the formation of new vessels, angiogenesis, and/or to be mitogenic for cultured endothelial cells. These factors include polypeptide growth factors-i.e., basic and acidic fibroblast growth factor (bFGF, aFGF)-endothelial cell growth factor, which is a precursor form of aFGF, transforming growth factors a and /3, angiogenin, and tumor necrosis factor a (1).Angiogenic factors may be important when released locally by cells adjacent to the endothelium, possibly also produced by the endothelial cells themselves or as circulating factors in plasma.Indirect evidence has suggested trophic effects of peripheral neurons. In the newt, naturally occurring limb regeneration is prevented by damage to the peripheral nerve innervating the limb (2). Intact sensory innervation has been shown to be important for corneal wound healing in the rat (3), and in humans suffering from Parry-Romberg syndrome, a marked hemifacial dystrophia is observed in the area innervated by the trigeminal nerve (4). Although direct evidence from in vivo studies is essentially lacking, recent studies have shown that sensory neuropeptides regulate cell proliferation in vitro. Neurokinin A (NKA) and substance P (SP), which are structurally related, have been shown to induce proliferation of human fibroblasts and rat smooth muscle cells (5). This effect was shown to be parallel with increased phosphatidylinositol (PI) turnover (6). Furthermore, vasoactive intestinal polypeptide (VIP) has been shown to inhibit serum-induced proliferation of rat smooth muscle cells and to stimulate prol...

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“…In human dermal capillary cells, CT and the phosphodiesterase inhibitor isobutylmethylxanthine have been shown to stimulate cell proliferation (35).…”

Section: Discussionmentioning

confidence: 99%

Calcitonin gene-related peptide stimulates proliferation of human endothelial cells.

Hægerstrand

Dalsgaard²,

Jonzon³

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

263

118

View full text Add to dashboard Cite

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“…Supernatants with nonbound cells were transferred to clean tubes and the separation was repeated to remove any remaining beads. Bound and nonbound cells were collected in EBM-MV2 Bulletkit culture median (Clonetics, BioWhittaker, Verviers, Belgium) with 0.5 M cAMP (Sigma) (Davison and Karasek, 1981). Nonpurified, purified (nonbound), and removed (bound) cells were seeded (10 5 /cm 2 ) on human fibronectin-coated culture plates.…”

Section: Thrombosis and Hemostasis Laboratory Department Of Hematolomentioning

confidence: 99%

A Novel Method for Isolating Pure Microvascular Endothelial Cells from Subcutaneous Fat Tissue Ideal for Direct Cell Seeding

Arts

Heijnen-Snyder

Joosten

et al. 2001

Laboratory Investigation

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“…Choleragen has been reported to stimulate proliferative growth in epidermal cells (19), endothelial cells (20), and mouse fibroblasts (7,21,22). Through study ofsequential events using PDGF and plasma, we recently demonstrated that the stimulatory action of choleragen and other agents elevating intracellular cAMP is on the early events associated with competence formation, since choleragen reduces the concentration of PDGF required for maximal (greater than 90%) stimulation of DNA synthesis in quiescent BALB/c-3T3 cells; i.e., it potentiates competence factors but is inactive alone or when added after competence formation during progression (7).…”

mentioning

confidence: 99%

Modulation of the epidermal growth factor receptor by platelet-derived growth factor and choleragen: Effects on mitogenesis

Wharton

Leof

Pledger

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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The addition of fresh medium supplemented with partially purified platelet-derived growth factor (PDGF) to quiescent density-arrested cultures of BALB/c-3T3 cells decreases the subsequent binding of radiolabeled epidermal growth factor (EGF). The decrease in EGF binding can be observed 1 hr after the addition of PDGF. This effect is maximal in 2-3 hr, and binding remains diminished for at least 6 hr. These effects can be accounted for by a decrease in the number of EGF receptors with no change in receptor affinity. The action of PDGF is concentration dependent, but even at very high concentrations of PDGF the reduction in EGF binding is never more than 50%. Similar decreases in EGF binding are produced by other treatments that render BALB/c-3T3 cells competent, such as the addition of fibroblast growth factor or medium previously exposed to the macrophage-like cell line P388D 1 . Cholera toxin (choleragen), which alone had no effect on EGF binding, dramatically potentiated the ability of PDGF to down regulate EGF receptors. Two to three hours after the addition of PDGF and choleragen, EGF binding was reduced by 80-90% compared with control values. The ability of PDGF and choleragen together to decrease EGF binding was substantially inhibited by cycloheximide. Autoradiography of [ 3 H]thymidine-labeled cells shows that choleragen potentiates the action of PDGF; lower concentrations of PDGF are required to make cells competent after choleragen treatment. Furthermore, cells treated with PDGF and choleragen no longer require EGF for traverse of G 1 phase and initiation of DNA synthesis in defined medium. The reduction in receptor number produced by choleragen and PDGF, which may be due to internalization of the EGF receptor, may mimic the action of EGF and thereby remove the EGF requirement for DNA synthesis.

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Human dermal microvascular endothelial cells in vitro: Effect of cyclic AMP on cellular morphology and proliferation rate

Cited by 88 publications

References 9 publications

Calcitonin gene-related peptide stimulates proliferation of human endothelial cells.

Calcitonin gene-related peptide stimulates proliferation of human endothelial cells.

A Novel Method for Isolating Pure Microvascular Endothelial Cells from Subcutaneous Fat Tissue Ideal for Direct Cell Seeding

Modulation of the epidermal growth factor receptor by platelet-derived growth factor and choleragen: Effects on mitogenesis

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