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Article

The Pathogenic Role of Smooth Muscle Cell-Derived Wnt5a in a Murine Model of Lung Fibrosis

1
Department of Molecular Immunology, Ruhr-University Bochum, 44780 Bochum, Germany
2
Department of Experimental Pneumology, Ruhr-University Bochum, 44780 Bochum, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Nektarios Barabutis
Pharmaceuticals 2021, 14(8), 755; https://0-doi-org.brum.beds.ac.uk/10.3390/ph14080755
Received: 1 July 2021 / Revised: 29 July 2021 / Accepted: 29 July 2021 / Published: 31 July 2021
(This article belongs to the Special Issue Lung Injury and Repair)
Idiopathic pulmonary fibrosis (IPF) is a disease characterized by extensive fibrosis of the lung tissue. Wnt5a expression was observed to be upregulated in IPF and suggested to be involved in the progression of the disease. Interestingly, smooth muscle cells (SMC) are a major source of Wnt5a in IPF patients. However, no study has been conducted until now to investigate the precise role of smooth muscle-derived Wnt5a in IPF. Here, we used the bleomycin-induced lung fibrosis model in a conditional gene-deficient mouse, where the Wnt5a gene was excised from SMC. We show here that the excision of the Wnt5a gene in SMC led to significantly improved health conditions with minimized weight loss and improved lung function. This improvement was based on a significantly lower deposition of collagen in the lung with a reduced number of fibrotic foci in lung parenchyma. Furthermore, the bleomycin-induced cellular infiltration into the airways was not altered in the gene-deficient mice compared with wild-type mice. Thus, we demonstrate that the Wnt5a expression of SMC of the airways leads to aggravated fibrosis of the lung with poor clinical conditions. This aggravation was not an influence in the bleomycin-induced inflammatory processes but on the development of fibrotic foci in lung parenchyma and the deposition of collagen. View Full-Text
Keywords: pulmonary fibrosis; bleomycin; Wingless-Type MMTV integration site family, member 5A; fibrotic foci; airway smooth muscle pulmonary fibrosis; bleomycin; Wingless-Type MMTV integration site family, member 5A; fibrotic foci; airway smooth muscle
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MDPI and ACS Style

Carmo-Fernandes, A.; Puschkarow, M.; Peters, K.; Gnipp, S.; Peters, M. The Pathogenic Role of Smooth Muscle Cell-Derived Wnt5a in a Murine Model of Lung Fibrosis. Pharmaceuticals 2021, 14, 755. https://0-doi-org.brum.beds.ac.uk/10.3390/ph14080755

AMA Style

Carmo-Fernandes A, Puschkarow M, Peters K, Gnipp S, Peters M. The Pathogenic Role of Smooth Muscle Cell-Derived Wnt5a in a Murine Model of Lung Fibrosis. Pharmaceuticals. 2021; 14(8):755. https://0-doi-org.brum.beds.ac.uk/10.3390/ph14080755

Chicago/Turabian Style

Carmo-Fernandes, André, Michelle Puschkarow, Karin Peters, Stefanie Gnipp, and Marcus Peters. 2021. "The Pathogenic Role of Smooth Muscle Cell-Derived Wnt5a in a Murine Model of Lung Fibrosis" Pharmaceuticals 14, no. 8: 755. https://0-doi-org.brum.beds.ac.uk/10.3390/ph14080755

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