Age-dependent changes in collagen metabolism and response to hypertonic culture conditions of rat aortic smooth muscle cells and skin fibroblasts

Hata, Ryu‐Ichiro

doi:10.1016/0309-1651(90)90068-a

Cited by 9 publications

(3 citation statements)

References 9 publications

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“…Because vessel wall synthesis occurs early in development, [25][26][27] collagen expression in neonatal animals was assessed. RNA was isolated from pooled aortas of neonatal (6 days old) WT and line 16 mice, and Northern blot analysis was performed ( Figure 1E).…”

Section: Neonatal Transgenic and Wt Mice Display Elevated Levels Of Cmentioning

confidence: 99%

“…Thus, cyclin A alleviates B-myb-mediated repression of the ␣1(I) collagen promoter, similar to its effects on the ␣2(V) promoter. 20 Because the bulk of matrix synthesis occurs early during development, [25][26][27] the presence of cyclin A likely explains, at least in part, why no significant differences were observed in collagen deposition in the vessel wall of transgenic animals.…”

Section: Neonatal Transgenic and Wt Mice Display Elevated Levels Of Cmentioning

confidence: 99%

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B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury

Hofmann

Sullivan²,

Jiang³

et al. 2004

ATVB

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Objectives-The function of B-Myb, a negative regulator of vascular smooth muscle cell (SMC) matrix gene transcription, was analyzed in the vasculature. Methods and Results-Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identified. Mice appeared to develop normally, and human B-myb was expressed in the aortas. Total B-Myb levels were elevated in aortas of adult transgenic versus wild-type (WT) animals and varied inversely with ␣1(I) collagen mRNA expression. However, neonatal WT and transgenic aortas displayed comparable levels of ␣1(I) collagen mRNA, likely resulting from elevated levels of cyclin A, which ablated repression by B-Myb. Aortic SMCs from adult transgenic animals displayed decreased ␣1(I) collagen mRNA levels. To examine the role of B-Myb after vascular injury, animals were subjected to femoral artery denudation, which induces SMC-rich lesion formation. A dramatic reduction in neointima formation and lumenal narrowing was observed in arteries of B-myb transgenic versus WT mice 4 weeks after injury. Key Words: Myb Ⅲ collagen Ⅲ cyclin A Ⅲ aorta Ⅲ femoral artery S mooth muscle cells (SMCs), the major cellular constituents of the medial layer of an artery, are responsible for synthesis and deposition of connective tissue proteins (including types I and V collagen, elastin, and proteoglycans) during artery development. 1 After the artery is formed, SMCs differentiate into a contractile phenotype. 1 During atherosclerosis development, a response to vascular injury is elicited. After monocyte invasion, SMCs migrate to the intima and dedifferentiate to a synthetic phenotype, displaying modest rounds of proliferation followed by matrix synthesis. 2,3 Deposition of matrix proteins, lipids, and minerals results in atherosclerotic plaque formation. Rupture of the fibrous cap of plaque with resultant exposure of thrombogenic subendothelial plaque constituents is the critical event that leads to thromboembolic complications in atherosclerotic coronary and carotid artery disease. [2][3][4] Atherosclerotic lesions are frequently treated by balloon angioplasty and stent placement. However, reoccurrence of arterial narrowing at the site of balloon angioplasty, termed restenosis, occurs in 30% to 50% of patients. 1 Acute disruption of the protective endothelial lining at the site of angioplasty appears to trigger excessive SMC hyperplastic responses, 5 extracellular matrix deposition, 3 and local vessel remodeling. 6,7 Cultured vascular SMCs from adult animals exhibit predominantly a synthetic phenotype, expressing genes encoding types I, III, and V/XI collagen at confluence or when deprived of serum growth factors, 8 -10 whereas during exponential growth, only low levels of matrix proteins are produced. Furthermore, basic fibroblast growth factor (bFGF), a potent inducer of SMC proliferation, decreased ␣1(I) and ␣2(V) collagen gene expression at the transcriptional level in bovine SMCs. 11 Overall, an inverse relationship exists between the p...

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Section: Neonatal Transgenic and Wt Mice Display Elevated Levels Of Cmentioning

confidence: 99%

Section: Neonatal Transgenic and Wt Mice Display Elevated Levels Of Cmentioning

confidence: 99%

B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury

Hofmann

Sullivan²,

Jiang³

et al. 2004

ATVB

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“…Variations in the relative rates of synthesis of extracellular matrix components were demonstrated in physiological as well as pathological conditions such as aging, UV radiations, a variety of skin diseases. Although total collagen synthesis decreases slowly with age [17,18], the relative proportion of collagen III was shown to increase with age and also in pathologies such as diabetes [19]. It could be shown that the biosynthesis of fibronectin increases with chronological age [20] and in vitro as a function of passage number of fibroblasts [16].…”

Section: Introductionmentioning

confidence: 99%

Effect of in vitro Aging on the Modulation of Protein and Fibronectin Biosynthesis by the Elastin-Laminin Receptor in Human Skin Fibroblasts

Fodil-Bourahla¹,

Drubaix²,

Robert³

et al. 1998

Gerontology

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The 67-kD elastin-laminin receptor (ELR) subunit which carries the recognition site for elastin peptides (EP) is a lectin. Its binding with galactosides can modulate the kinetics of its interaction with its ligand, EP. In this study the biosynthesis of proteins, collagen and fibronectin were evaluated in the presence of agonists and antagonists of the receptor on human skin fibroblasts. The biosynthesis of total proteins determined by ³H-proline incorporation and of fibronectin (by immunoprecipitation) were shown to increase with passage number. The presence of 1 µg/ml κ-elastin (EP) in the culture medium increased both total proteins and fibronectin biosynthesis. Melibiose, an agonist of the receptor at 5 µg/ml (140 µM), decreased both proteins and fibronectin biosynthesis in the culture medium of human skin fibroblast at the 10th and 15th passage. These results show that the ELR can control the biosynthetic mechanisms of some of the macromolecular constituents of extracellular matrix such as fibronectin and moderate its age and passage-dependent upregulation.

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Altered cellular responsiveness during ageing

Rattan

Derventzi

1991

BioEssays

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The capacity of cells and organisms to respond to external stimuli and to maintain stability in order to survive decreases progressively during ageing. The mitogenic and stimulatory effects of growth factors, hormones and other agents are reduced significantly during cellular ageing. The sensitivity of ageing cells to toxic agents including antibiotics, phorbol esters, radiations and heat shock increases. This failure of homeostasis during cellular ageing does not appear to be due to any quantitative and qualitative defects in the receptor systems. Instead, metabolic defects in the pathways of macromolecular synthesis may be the basis of altered cellular responsiveness during ageing.

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Age-dependent changes in collagen metabolism and response to hypertonic culture conditions of rat aortic smooth muscle cells and skin fibroblasts

Cited by 9 publications

References 9 publications

B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury

B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury

Effect of in vitro Aging on the Modulation of Protein and Fibronectin Biosynthesis by the Elastin-Laminin Receptor in Human Skin Fibroblasts

Altered cellular responsiveness during ageing

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