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Citations to this article

Rat lung fibroblast collagen metabolism in bleomycin-induced pulmonary fibrosis.
S H Phan, … , J Varani, D Smith
S H Phan, … , J Varani, D Smith
Published July 1, 1985
Citation Information: J Clin Invest. 1985;76(1):241-247. https://doi.org/10.1172/JCI111953.
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Research Article Article has an altmetric score of 3

Rat lung fibroblast collagen metabolism in bleomycin-induced pulmonary fibrosis.

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Abstract

Endotracheal bleomycin administration in rats and other animal species causes rapid development of pulmonary fibrosis, characterized by increased lung collagen synthesis and deposition. To clarify the mechanism, lung fibroblasts from bleomycin-treated rats (BRF) were isolated and maintained in tissue culture. They were then compared with those from normal untreated control animals, with respect to several key parameters of collagen metabolism. BRF synthesized collagen at a rate 35-82% above normal rat lung fibroblasts (NRF). This difference did not appear to be due to the selection of a clone by the subculture process. Furthermore, analysis of newly synthesized collagen type composition, revealed a significantly lower ratio of type III to type I collagen. Noncollagenous protein synthesis, however, was not significantly different from normal. Collagenase production and growth rate were also unaffected. BRF, however, was morphologically indistinguishable from NRF, even at the ultrastructural level. Upon further bleomycin (1 microgram/ml) exposure in vitro, BRF could be further stimulated to synthesize collagen at 82% above the rate for untreated BRF. This is comparable to the 90% increase in NRF treated in vitro (compared with untreated NRF). These results would favor the conclusion that bleomycin induces pulmonary fibrosis, by causing directly and/or indirectly lung fibroblasts (or a certain line of lung fibroblasts) to synthesize collagen at a higher rate without any associated increase in growth rate. The data, however, do not rule out the possibility that the fibroblast isolation procedure has selected for a certain population of fibroblasts that may not be typical of the in vivo situation.

Authors

S H Phan, J Varani, D Smith

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Citations to this article in year 2012 (6)

Title and authors Publication Year
Cardiopulmonary dysfunction in the Osteogenesis imperfecta mouse model Aga2 and human patients are caused by bone-independent mechanisms
F Thiele, CM Cohrs, A Flor, TS Lisse, GK Przemeck, M Horsch, A Schrewe, V Gailus-Durner, B Ivandic, HA Katus, W Wurst, C Reisenberg, H Chaney, H Fuchs, W Hans, J Beckers, JC Marini, MH de Angelis
Human Molecular Genetics 2012
Encyclopedia of Drug Metabolism and Interactions
M Fielden, C Karbowski
Encyclopedia of Drug Metabolism and Interactions 2012
Vapor of volatile oils from Litsea cubeba seed induces apoptosis and causes cell cycle arrest in lung cancer cells
S Seal, P Chatterjee, S Bhattacharya, D Pal, S Dasgupta, R Kundu, S Mukherjee, S Bhattacharya, M Bhuyan, PR Bhattacharyya, G Baishya, NC Barua, PK Baruah, PG Rao, S Bhattacharya
PloS one 2012
Involvement of Endoplasmic Reticulum Stress in Myofibroblastic Differentiation of Lung Fibroblasts
HA Baek, DS Kim, HS Park, KY Jang, MJ Kang, DG Lee, WS Moon, HJ Chae, MJ Chung
American journal of respiratory cell and molecular biology 2012
Vascular dysfunction by myofibroblast activation in patients with idiopathic pulmonary fibrosis and prognostic significance
ER Parra, R Falzoni, VL Capelozzi
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 2012
Transforming growth factor-β regulates endothelin-1 signaling in the newborn mouse lung during hypoxia exposure
N Olave, T Nicola, W Zhang, A Bulger, M James, S Oparil, YF Chen, N Ambalavanan
American journal of physiology. Lung cellular and molecular physiology 2012

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