Corticosteroids increase procollagen gene expression, synthesis, and secretion by human intestinal smooth muscle cells

Graham, Martin F.; Willey, Amy; Adams, John W.; Diegelmann, Robert F.

doi:10.1016/0016-5085(95)90630-4

Cited by 35 publications

(32 citation statements)

References 21 publications

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“…Their expression at the mRNA and protein levels continued after expression of inflammation-related genes had resumed basal levels. Earlier studies have also linked altered amounts of collagen I and III with fibrosis (38,(47)(48)(49). Increase in the ECM protein lumican (Lum) in colitis was a novel finding.…”

Section: Discussionmentioning

confidence: 86%

Differential Expression of Inflammatory and Fibrogenic Genes and Their Regulation by NF-κB Inhibition in a Mouse Model of Chronic Colitis

Chakravarti

2007

The Journal of Immunology

111

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Fibrosis is a major complication of chronic inflammation, as seen in Crohn's disease and ulcerative colitis, two forms of inflammatory bowel diseases. To elucidate inflammatory signals that regulate fibrosis, we investigated gene expression changes underlying chronic inflammation and fibrosis in trinitrobenzene sulfonic acid-induced murine colitis. Six weekly 2,4,6-trinitrobenzene sulfonic acid enemas were given to establish colitis and temporal gene expression patterns were obtained at 6-, 8-, 10-, and 12-wk time points. The 6-wk point, TNBS-w6, was the active, chronic inflammatory stage of the model marked by macrophage, neutrophil, and CD3؉ and CD4 ؉ T cell infiltrates in the colon, consistent with the idea that this model is T cell immune response driven. Proinflammatory genes Cxcl1, Ccl2, Il1b, Lcn2, Pla2g2a, Saa3, S100a9, Nos2, Reg2, and Reg3g, and profibrogenic extracellular matrix genes Col1a1, Col1a2, Col3a1, and Lum (lumican), encoding a collagen-associated proteoglycan, were up-regulated at the active/chronic inflammatory stages. Rectal administration of the NF-B p65 antisense oligonucleotide reduced but did not abrogate inflammation and fibrosis completely. The antisense oligonucleotide treatment reduced total NF-B by 60% and downregulated most proinflammatory genes. However, Ccl2, a proinflammatory chemokine known to promote fibrosis, was not downregulated. Among extracellular matrix gene expressions Lum was suppressed while Col1a1 and Col3a1 were not. Thus, effective treatment of fibrosis in inflammatory bowel disease may require early and complete blockade of NF-B with particular attention to specific proinflammatory and profibrogenic genes that remain active at low levels of NF-B.

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Section: Discussionmentioning

confidence: 86%

Differential Expression of Inflammatory and Fibrogenic Genes and Their Regulation by NF-κB Inhibition in a Mouse Model of Chronic Colitis

Chakravarti

2007

The Journal of Immunology

111

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“…Fluticasone uptake was not able to reduce basal membrane thickness after 8 wk of treatment (8). Glucocorticoids increased procollagen synthesis by intestinal and vascular smooth muscle cells (19,28). Dex increased procollagen I synthesis by primary bronchial fibroblasts when stimulated with ET-1, PDGF, and TGF-␤ (15).…”

Section: Discussionmentioning

confidence: 99%

AP-1 overexpression impairs corticosteroid inhibition of collagen production by fibroblasts isolated from asthmatic subjects

Jacques

Semlali

Boulet

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Usage, even for a short period, can induce hypertension [10,13]. Furthermore, corticosteroids have an influence on the constitution of the arterial vessel wall as the formation of collagen, an important constituent of the arterial vessel wall, is affected by corticosteroids [2,3,9]. Corticosteroids control collagen production, resulting in an inhibition of the collagen synthesis [3].…”

Section: Introductionmentioning

confidence: 99%

“…Corticosteroids control collagen production, resulting in an inhibition of the collagen synthesis [3]. In addition, corticosteroids decrease the type III/type I collagen ratio [2] and increase the haemodynamic strain of the blood vessels by increasing the stiffness of the vessel [9].…”

Section: Introductionmentioning

confidence: 99%

Corticosteroid use and risk of aneurysmal subarachnoid haemorrhage

et al. 2005

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Corticosteroids increase procollagen gene expression, synthesis, and secretion by human intestinal smooth muscle cells

Cited by 35 publications

References 21 publications

Differential Expression of Inflammatory and Fibrogenic Genes and Their Regulation by NF-κB Inhibition in a Mouse Model of Chronic Colitis

Differential Expression of Inflammatory and Fibrogenic Genes and Their Regulation by NF-κB Inhibition in a Mouse Model of Chronic Colitis

AP-1 overexpression impairs corticosteroid inhibition of collagen production by fibroblasts isolated from asthmatic subjects

Corticosteroid use and risk of aneurysmal subarachnoid haemorrhage

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