Increased mRNA expression of collagen V gene in pulmonary fibrosis of systemic sclerosis

Parra, Edwin Roger; Teodoro, W. R.; Morais, Jymenez de; Katayama, Maria Lúcia Hirata; Souza, R De; Nh, Yoshinari; Capelozzi, Vera Luíza

doi:10.1111/j.1365-2362.2009.02224.x

Cited by 17 publications

(14 citation statements)

References 32 publications

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“…MCP-6, one of the mast cell-derived granule components, is the counterpart of human tryptase because of its predicted tryptic-like substrate specificity (18,22). Collagen V consists of about 1-5% of the total collagens in healthy tissue; however, it increases during fibrogenesis in liver (31) and lung (20), playing an anchoring role between collagen fibrils (31,32). Collagen V is also reported to increase in obese adipose tissue (10,25), especially in fibrotic areas (26).…”

Section: Discussionmentioning

confidence: 99%

Involvement of mast cells in adipose tissue fibrosis

Hirai

Ohyane

Kim

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Recently, fibrosis is observed in obese adipose tissue; however, the pathogenesis remains to be clarified. Obese adipose tissue is characterized by chronic inflammation with massive accumulation of immune cells including mast cells. The objective of the present study was to clarify the relationship between fibrosis and mast cells in obese adipose tissue, as well as to determine the origin of infiltrating mast cells. We observed the enhancement of mast cell accumulation and fibrosis in adipose tissue of severely obese diabetic db/db mice. Furthermore, adipose tissue-conditioned medium (ATCM) from severely obese diabetic db/db mice significantly enhanced collagen 5 mRNA expression in NIH-3T3 fibroblasts, and this enhancement was suppressed by the addition of an anti-mast cell protease 6 (MCP-6) antibody. An in vitro study showed that only collagen V among various types of collagen inhibited preadipocyte differentiation. Moreover, we found that ATCM from the nonobese but not obese stages of db/db mice significantly enhanced the migration of bone marrow-derived mast cells (BMMCs). These findings suggest that immature mast cells that infiltrate into adipose tissue at the nonobese stage gradually mature with the progression of obesity and diabetes and that MCP-6 secreted from mature mast cells induces collagen V expression in obese adipose tissue, which may contribute to the process of adipose tissue fibrosis. Induction of collagen V by MCP-6 might accelerate insulin resistance via the suppression of preadipocyte differentiation.

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Section: Discussionmentioning

confidence: 99%

Involvement of mast cells in adipose tissue fibrosis

Hirai

Ohyane

Kim

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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“…Disordered COLV fibrillar architecture . COLV is normally distributed in the alveolar septa, walls of bronchi, terminal bronchioles, and blood vessels, albeit in smaller amounts relative to fibrillar COLI or III (Parra et al, ). COLV is causal for the pathogenesis of pulmonary interstitial fibrosis, such as idiopathic pulmonary fibrosis (IPF) (Parra et al, ) and pulmonary fibrosis of systemic sclerosis (SS) (Parra et al, ).…”

Section: Disease and Fibrosismentioning

confidence: 99%

“…COLV is normally distributed in the alveolar septa, walls of bronchi, terminal bronchioles, and blood vessels, albeit in smaller amounts relative to fibrillar COLI or III (Parra et al, ). COLV is causal for the pathogenesis of pulmonary interstitial fibrosis, such as idiopathic pulmonary fibrosis (IPF) (Parra et al, ) and pulmonary fibrosis of systemic sclerosis (SS) (Parra et al, ). In lung biopsies of IPF patients—with a histological pattern of usual interstitial pneumonia—and SS patients, COLV expression is strikingly increased in the alveolar septa and pre‐acinar arterial walls in parallel with the severity of the fibrotic lesion, as assessed by immunohistochemistry.…”

Section: Disease and Fibrosismentioning

confidence: 99%

“…Moreover, histomorphometry revealed that COLV deposition coincident with COLI in fibrotic foci is disarrayed, showing increased density and thickness. In the lung, the COLV isoform containing the α1(V) 2 α2(V) heterotrimer is predominant (Parra et al, ). The authors found that the lung biopsies of patients with SS have higher mRNA expression for α1(V) and α2(V) chains with a striking sevenfold increase of the α2(V) mRNA.…”

Section: Disease and Fibrosismentioning

confidence: 99%

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Type V Collagen in Health, Disease, and Fibrosis

Mak

Png

Lee

2016

The Anatomical Record

137

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Type V collagen (COLV) is a regulatory fibril-forming collagen. It has at least three different molecular isoforms-a1(V) 2 a2(V), a1(V) 3, and a1(V)a2(V)a3(V)-formed by combinations of three different polypeptide a chains-a1(V), a2(V), and a3(V). COL V is a relatively minor collagen of the extracellular matrix (ECM). Morphologically, COLV occurs as heterotypic fibrils with type I collagen (COLI), microfilaments, or 12-nm-thick fibrils. COLV is synthesized in various mesenchymal cells and its gene expression is modulated by TGF-b and growth factors. While resistant to digestion by interstitial collagenases, native and denatured COLV are degraded by metalloproteinases and gelatinases, thereby promoting ECM remodeling. COLV interacts with matrix collagens and structural proteins, conferring structural integrity to tissue scaffolds. It binds matrix macromolecules, modulating cellular behavior, and functions. COLV coassembles with COLI into heterotypic fibrils in the cornea and skin dermis, acting as a dominant regulator of collagen fibrillogenesis. COLV deficiency is associated with loss of corneal transparency and classic EhlersDanlos syndrome, while COLV overexpression is found in cancer, granulation tissue, inflammation, atherosclerosis, and fibrosis of lungs, skin, kidneys, adipose tissue, and liver. COLV isoform containing the a3(V) chain is involved in mediating pancreatic islet cell functions. In the liver, COLV is a minor but regular component of the ECM. Increases in COLV are associated with both early and advanced hepatic fibrosis. The neoepitopes of COLV have been shown to be a useful noninvasive serum biomarker for assessing fibrotic progression and resolution in experimental hepatic fibrosis. COLV is multifunctional in health, disease, and fibrosis. Anat Rec, 299:613-629, 2016. V C 2016 Wiley Periodicals, Inc.Key words: collagen V synthesis and degradation; collagen V deficiency and overexpression; collagen V in disease and fibrosis; collagen V neoepitopes; hepatic fibrosis biomarker

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“…indicando que esta proteína tem um papel nos distúrbios fibróticos do tecido pulmonar(Parra et al, 2009;Parra et al, 2010). Mais recentemente, Fabro et al…”

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Modulação do microambiente periférico pelas células-tronco mesenquimais e meio condicionado na fibrose pulmonar experimental

Felix¹

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Dedico este trabalho a Deus: o médico dos médicos. AGRADECIMENTOS Agradeço a Deus e a todos aqueles que me apoiaram e participaram desta maravilhosa etapa da minha vida, em especial: À minha amada esposa, Natália Regina Gerlin Felix, por todo amor, pela compreensão e pelo companheirismo. À minha dedicada mãe, Marlene Gonçalves Felix, e a meu irmão, Adriano Gonçalves Felix, por todo incentivo, pelo apoio e pelo enorme afeto. À Profa. Dra. Vera Luiza Capelozzi, por ter aceitado o desafio de orientar meu trabalho, e por ter tanta paciência e determinação para transferir seu conhecimento. À Profa. Dra. Elenice Deffune, por ter aceitado dar continuidade ao meu aprendizado, e orientar meu desenvolvimento acadêmico e humano. Ao Prof. Dr. Alexandre Todorovic Fabro, por ter aceitado orientar minha pesquisa e por ser um exemplo de lealdade, determinação e perseverança. À Profa. Dra. Giesela Fleischer Ferrari, por ter me preparado, me incentivado e me ensinado muito do que aprendi no caminho da docência. À Drª. Marjorie de Assis Golim, por todo o apoio e pelos conhecimentos transmitidos, e, sobretudo, pela dedicação demonstrada. À Sra. Ondina Silvia Cotrim, pela pró-atividade, impressionante dedicação e pronta ajuda sempre que necessário. À Srta. Ana Lívia de Carvalho Bovolato, pelo apoio, pela parceria, pela importantíssima ajuda durante esta jornada e por sua grande dedicação. Ao Bioterista Paulo César, pela experiência, pela dedicação e pelo carinho no cuidado com nossos animais no biotério. As Srtas. Patricia Leão e Juliana Machado, pela colaboração e pela dedicação demonstradas. Aos demais amigos e funcionários dos laboratórios de Engenharia Celular e de Patologia que tive a honra de conviver e trabalhar no período de 2015 a 2018. Muito obrigado! NORMALIZAÇÃO ADOTADA Esta tese está de acordo com as seguintes normas, em vigor no momento desta publicação: Referências: adaptado de International Committee of Medical Journals Editors (Vancouver).

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Increased mRNA expression of collagen V gene in pulmonary fibrosis of systemic sclerosis

Cited by 17 publications

References 32 publications

Involvement of mast cells in adipose tissue fibrosis

Involvement of mast cells in adipose tissue fibrosis

Type V Collagen in Health, Disease, and Fibrosis

Modulação do microambiente periférico pelas células-tronco mesenquimais e meio condicionado na fibrose pulmonar experimental

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