The elastogenic effect of recombinant transforming growth factor-beta on porcine aortic smooth muscle cells

Liu, Ji-min; Davidson, Jeffrey M.

doi:10.1016/0006-291x(88)90224-0

Cited by 125 publications

(49 citation statements)

References 21 publications

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“…The role of this factor in the physiologic perinatal adaptation and growth of the pulmonary vasculature is not known. TGF-P is another candidate because it increases in the vascular wall in response to hypertension (16) and could in turn increase TE synthesis (17). However, Botney et al (1 8) recently reported in a preliminary form that the normal rise in TGF-6 mRNA was not seen in the PA of the pulmonary hypertensive calf.…”

Section: Resultsmentioning

confidence: 99%

Tropoelastin Gene Expression in the Rat Pulmonary Vasculature: A Developmental Study

1992

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ABSTRACT. The elastic laminae in a vessel provide resilience to its wall. In perinatal and adult rats, we used in situ hybridization to localize the mRNA for tropoelastin (TE) in endothelial cells, medial smooth muscle cells, and adventitial fibroblasts of pulmonary arteries and veins to determine the contribution of these cells to laminae formation. We found that 1 ) all three cell types are elastogenic but for each the ontogenic pattern is different, 2) signal in the artery is strongest in the late fetal lung, 3) postnatally TE expression decreases first in the outer medial smooth muscle cells, and 4) the pattern of expression in arteries differs from that in veins. In the d 19 fetus, the signal for TE mRNA was higher in arteries than in veins. In the immediate postnatal period, the arterial signal declined, whereas the signal in veins increased. By postnatal d 21, the arterial TE signal per cell had significantly decreased to an intensity lower than that in veins. In the adult rat lung, no TE mRNA was detected by in situ hybridization. The reciprocal alterations in TE expression in pulmonary arteries and veins may suggest a response to the postnatal change in pulmonary blood pressure. We speculate that because all three cell types are potentially elastogenic they may all play a role in the remodeling that occurs after vascular injury. (Pediatr Res 31: 280-285, 1992) Abbreviations ISH, in situ hybridization TE, tropoelastin SSC, sodium chloride sodium citrate buffer RT, room temperature PA, pulmonary artery PV, pulmonary vein TGF-B, transforming growth factor+The resilience of the vascular wall is attributed largely to its elastic laminae. Synthesis of the elastin pro-protein, TE, by vascular smooth muscle cells has been demonstrated in tissues ( 1-4) and isolated cells (3,5,6). We have recently demonstrated the specificity of the TE complementary RNA probe and identified, by ISH, TE mRNA in endothelial cells of the rat preacinar PA in perinatal lung tissue (7). Although elastogenesis in pulmonary vascular cells is developmentally regulated (8) as in other tissues, the dramatic changes of pulmonary blood pressure and oxygenation at birth may be significant regulatory factors. Prosser et al. (9) have shown by ISH that there is increased TE mRNA in the medial smooth muscle cells of the hypoxia-induced pulmonary hypertensive calf compared with normotensive controls. With the physiologic postnatal drop in pulmonary arteriolar resistance, PA pressure decreases and PV pressure and flow rise concomitantly. To study the relative contribution of endothelial cells, smooth muscle cells, and adventitial fibroblasts to the formation of elastic laminae during normal perinatal pulmonary vascular adaptation and growth, we evaluated in perinatal rat pups TE mRNA distribution in the main PA, in preacinar and intraacinar arteries, and in postacinar and lobular PV. We found that TE expression decreases in the PA and increases in the PV postnatally and that endothelial cells, smooth muscle cells, and adventitial fibroblasts all...

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Section: Resultsmentioning

confidence: 99%

Tropoelastin Gene Expression in the Rat Pulmonary Vasculature: A Developmental Study

1992

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“…Transforming growth factor-β (TGF-β) plays an important part in the pathogenesis of fibrosis, since these peptides stimulate the production of extracellular matrix (Fine and Goldstein, 1987;Liu and Davidson, 1988) and inhibit the formation of extracellular proteases (Keski-Oja et al, 1988). We think that the proliferation of connective tissue elements such as fibroblasts, fibrocytes and extracellular matrix in the canine lipoma was a non-neoplastic, reactive consequence of the secretion of transforming growth factor-β 1 (TGF-β 1 ) (Pennington et al, 1992a) and other growth factors for fibroblasts by mast cells (Pennington et al, 1992b).…”

Section: Discussionmentioning

confidence: 99%

Cutaneous mast cell tumour within a lipoma in a boxer

Jakab

Szász

Kulka

et al. 2009

Acta Veterinaria Hungarica

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This report describes a case of a canine cutaneous grade I mast cell tumour which developed within a lipoma in the right axillar region of an 8-year-old male Boxer. Immunohistologically, the neoplastic mast cells were positive for serotonin, CD45 vimentin and p53, and negative for lysozyme, CD3 and CD79a expression. The proliferation index of the mast cell tumour based on the Ki-67 antigen was 6.1%. Between the benign neoplastic lipocytes and mastocytoma tumour cells intratumoural microvessels were detected by immunohistochemical staining using CD31 and claudin-5 as markers for vascular endothelium.

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“…Several factors secreted by macrophages (1O, I ) are capable of stimulating extracellular matrix protein synthesis. TGF-f3, stimulates production of fibronectin ( 12, 13), collagen ( 14,15), and tropoelastin ( 16,17). IGF induces the synthesis oftropoelastin (18)(19)(20), and type I collagen (21 ).…”

Section: Introductionmentioning

confidence: 99%

Neointimal macrophages colocalize with extracellular matrix gene expression in human atherosclerotic pulmonary arteries.

Liptay¹,

Parks²,

Mecham³

et al. 1993

J. Clin. Invest.

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Vascular remodeling in adult atherosclerotic pulmonary arteries is characterized by discrete areas of neointimal extracellular matrix gene expression, suggesting regulation by local factors. Though the factors responsible for inducing matrix gene expression in atherosclerotic lesions are largely unknown, several observations suggest macrophages may be a focal source of those factors.Immunohistochemistry confirmed the presence of macrophages in the neointima of atherosclerotic elastic pulmonary arteries from patients with unexplained pulmonary hypertension. Areas of neointima containing dense clusters of macrophages were separated by sparsely populated areas. Foamy macrophages resided more deeply within the neointima than nonfoamy macrophages, which were found more often subjacent to the endothelium or within the lumenal one-third of the neointima. Combined immunohistochemistry-in situ hybridization indicated neointimal fibronectin and type I procollagen gene expression was intimately associated only with nonfoamy neointimal macrophages.These observations suggest that: (a) nonfoamy neointimal macrophages participate in the local regulation of extracellular matrix gene expression in atherosclerotic pulmonary arteries; (b) foamy macrophages, which are not associated with matrix gene expression, have undergone modulation of their secretory phenotype. (J. Clin. Invest. 1993. 91:588-594.)

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The elastogenic effect of recombinant transforming growth factor-beta on porcine aortic smooth muscle cells

Cited by 125 publications

References 21 publications

Tropoelastin Gene Expression in the Rat Pulmonary Vasculature: A Developmental Study

Tropoelastin Gene Expression in the Rat Pulmonary Vasculature: A Developmental Study

Cutaneous mast cell tumour within a lipoma in a boxer

Neointimal macrophages colocalize with extracellular matrix gene expression in human atherosclerotic pulmonary arteries.

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