Modulation of the
            <i>sis</i>
            Gene Transcript During Endothelial Cell Differentiation in Vitro

Jaye, Michael; McConathy, Evelyn; Drohan, William N.; Tong, Benton D.; Deuel, Thomas F.; Maciag, Thomas

doi:10.1126/science.3890179

Cited by 105 publications

(38 citation statements)

References 23 publications

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“…For example, bovine aortic or human umbilical vein endothelial cells stripped from blood vessels contain only 10% and 1.3%, respectively, as much Bchain transcript as the same cells in monolayer culture (28). When endothelium switches from a monolayer to tubelike structures in culture it alters its expression of A-and B-chain mRNA (29)(30)(31). Transient expression of PDGF is induced in response to cell activation by coagulation factors and by cytokines, as well as by variations in cell substrate (1,12,27).…”

Section: Discussionmentioning

confidence: 99%

Platelet-derived growth factor activity and mRNA expression in healing vascular grafts in baboons. Association in vivo of platelet-derived growth factor mRNA and protein with cellular proliferation.

Golden¹,

Au²,

Kirkman³

et al. 1991

J. Clin. Invest.

117

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In a baboon graft model of arterial intimal thickening, smooth muscle cells (SMC) have been observed to proliferate underneath an intact monolayer of endothelium and in the absence of platelet adherence. Because platelets are not present and therefore cannot be a major source of growth stimulus, we have proposed that the vascular wall cells in the graft intima express mitogens and regulate SMC proliferation. To test this hypothesis, we assayed the grafts for mitogenic activity and expression of growth factor genes. Segments of healing graft and of normal artery, when perfused ex vivo, released mitogenic activity into the perfusate. The graft released more mitogen than the normal arterial segment, and some of the activity was inhibitable with an antibody to human platelet-derived growth factor (PDGF). In addition, Northern analysis of total RNA demonstrated higher expression of PDGF-A chain mRNA in the graft intima compared to normal artery. PDGF-B chain mRNA was barely detectable in both tissues. PDGF mRNA levels within the graft interstices were not measured. In situ hybridization of 7.5-or 12-wk grafts indicated that some luminal endothelial cells and adjacent intimal SMC contained PDGF-A chain mRNA. By thymidine autoradiography, intimal SMC were observed to be proliferating in the inner third of the intima. These data demonstrate a difference in the pattern of PDGF transcript expression and luminal perfusate activity in graft as compared with control arteries. The association of intimal smooth muscle cell proliferation with intimal PDGF mRNA expression and release of PDGF-like protein supports the hypothesis that factors from cells that have grown into the graft or populated its surface rather than platelets may regulate intimal smooth muscle cell proliferation in this model. (J. Clin. Invest. 1991. 87:406-414.)

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Section: Discussionmentioning

confidence: 99%

Platelet-derived growth factor activity and mRNA expression in healing vascular grafts in baboons. Association in vivo of platelet-derived growth factor mRNA and protein with cellular proliferation.

Golden¹,

Au²,

Kirkman³

et al. 1991

J. Clin. Invest.

117

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“…The differential plating density was implemented to study experimental and control cells in the same assay at the same final density. This was not otherwise achievable owing to the replicative delay induced by high glucose (10, 1 1), and yet desirable when studying the level of fibronectin mRNA, known to be modulated by the proliferative state ofendothelial cells (16). Cells were cultured as described (10) in medium 199 (Gibco Laboratories, Grand Island, NY) supplemented with 2 mM glutamine, 17.5 mM Hepes buffer, 14%…”

Section: Methodsmentioning

confidence: 99%

Increased expression of basement membrane components in human endothelial cells cultured in high glucose.

Cagliero

Maiello²,

Boeri³

et al. 1988

J. Clin. Invest.

187

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Although the degree of hyperglycemia is a powerful and independent risk factor for diabetic microvascular disease, it has not been established if and how high glucose per se can induce the typical lesions of microangiopathy. We have investigated in human vascular endothelial cells the expression of messenger RNA (mRNA) for collagen type IV and fibronectin, the two glycoproteins characteristically increased in diabetic basement membranes. In 12 confluent primary cultures exposed for 11±14 (mean±SD) to 30 mM glucose and exhibiting cell number and thymidine incorporation similar to control cultures, the levels of collagen IV and fibronectin mRNA were, respectively, 238±140 and 221±231 percent of control (P < 0.01). The effects of high glucose were selective (the levels of collagen I and c-myc mRNA remained unchanged), independent of the proliferative activity of the cultures and of the plating substratum, and maintained throughout multiple passages. However, several days of exposure to high glucose were required before their appearance. These observations establish that high glucose is a perturbation sufficient to mimic the effects of diabetes on the regulation of basement membrane components and propose that modifications in gene expression may pertain to the chain of events leading to diabetic angiopathy.

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“…However, the critical source of PDGFB in the process of VSMC/PC recruitment is not firmly established. Endothelial cells have been shown to express PDGFB in vitro (Jaye et al, 1985) and in vivo (Hellström et al, 1999;Lindahl et al, 1997), suggesting that PC recruitment is controlled by short-range PDGFB/PDGFRβ signaling between the endothelium and the PCs. However, several other cell types express PDGFB, for example megakaryocytes/platelets and monocytes/ macrophages (Heldin and Westermark, 1999).…”

Section: Introductionmentioning

confidence: 99%

Endothelium-specific ablation of PDGFB leads to pericyte loss and glomerular, cardiac and placental abnormalities

et al. 2004

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Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development, but the relative importance of different cellular sources of PDGFB has not been established. Using Cre-lox techniques, we show here that genetic ablation of Pdgfb in endothelial cells leads to impaired recruitment of pericytes to blood vessels. The endothelium-restricted Pdgfb knockout mutants also developed organ defects including cardiac, placental and renal abnormalities. These defects were similar to those observed in Pdgfb null mice. However, in marked contrast to the embryonic lethality of Pdgfb null mutants, the endothelium-specific mutants survived into adulthood with persistent pathological changes, including brain microhemorrhages, focal astrogliosis, and kidney glomerulus abnormalities. This spectrum of pathological changes is reminiscent of diabetic microangiopathy, suggesting that the endothelium-restricted Pdgfb knockouts may serve as models for some of the pathogenic events of vascular complications to diabetes.

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Modulation of the sis Gene Transcript During Endothelial Cell Differentiation in Vitro

Cited by 105 publications

References 23 publications

Platelet-derived growth factor activity and mRNA expression in healing vascular grafts in baboons. Association in vivo of platelet-derived growth factor mRNA and protein with cellular proliferation.

Platelet-derived growth factor activity and mRNA expression in healing vascular grafts in baboons. Association in vivo of platelet-derived growth factor mRNA and protein with cellular proliferation.

Increased expression of basement membrane components in human endothelial cells cultured in high glucose.

Endothelium-specific ablation of PDGFB leads to pericyte loss and glomerular, cardiac and placental abnormalities

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