Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.

Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite involved in many critical cellular processes, including proliferation, migration, and angiogenesis, through interaction with a family of five G protein-coupled receptors (S1P1-5). Some reports have implicated S1P as an important in...

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Autores principales:	Ken Murakami, Masataka Kohno, Masatoshi Kadoya, Hidetake Nagahara, Wataru Fujii, Takahiro Seno, Aihiro Yamamoto, Ryo Oda, Hiroyoshi Fujiwara, Toshikazu Kubo, Satoshi Morita, Hiroshi Nakada, Timothy Hla, Yutaka Kawahito
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/172555b6a02d4e149684be58e8f01622
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spelling	oai:doaj.org-article:172555b6a02d4e149684be58e8f016222021-11-25T06:01:29ZKnock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.1932-620310.1371/journal.pone.0106792https://doaj.org/article/172555b6a02d4e149684be58e8f016222014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25198418/?tool=EBIhttps://doaj.org/toc/1932-6203Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite involved in many critical cellular processes, including proliferation, migration, and angiogenesis, through interaction with a family of five G protein-coupled receptors (S1P1-5). Some reports have implicated S1P as an important inflammatory mediator of the pathogenesis of airway inflammation, but the role of S1P3 in the pathogenesis of lung diseases is not completely understood. We used S1P3-deficient (knockout (KO)) mice to clarify the role of S1P3 receptor signaling in the pathogenesis of pulmonary inflammation and fibrosis using a bleomycin-induced model of lung injury. On the seventh day after bleomycin administration, S1P3 KO mice exhibited significantly less body weight loss and pulmonary inflammation than wild-type (WT) mice. On the 28th day, there was less pulmonary fibrosis in S1P3 KO mice than in WT mice. S1P3 KO mice demonstrated a 56% reduction in total cell count in bronchoalveolar lavage fluid (BALF) collected on the seventh day compared with WT mice; however, the differential white blood cell profiles were similar. BALF analysis on the seventh day showed that connective tissue growth factor (CTGF) levels were significantly decreased in S1P3 KO mice compared with WT mice, although no differences were observed in monocyte chemotactic protein-1 (MCP-1) or transforming growth factor β1 (TGF-β1) levels. Finally, S1P levels in BALF collected on the 7th day after treatment were not significantly different between WT and S1P3 KO mice. Our results indicate that S1P3 receptor signaling plays an important role in pulmonary inflammation and fibrosis and that this signaling occurs via CTGF expression. This suggests that this pathway might be a therapeutic target for pulmonary fibrosis.Ken MurakamiMasataka KohnoMasatoshi KadoyaHidetake NagaharaWataru FujiiTakahiro SenoAihiro YamamotoRyo OdaHiroyoshi FujiwaraToshikazu KuboSatoshi MoritaHiroshi NakadaTimothy HlaYutaka KawahitoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e106792 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ken Murakami Masataka Kohno Masatoshi Kadoya Hidetake Nagahara Wataru Fujii Takahiro Seno Aihiro Yamamoto Ryo Oda Hiroyoshi Fujiwara Toshikazu Kubo Satoshi Morita Hiroshi Nakada Timothy Hla Yutaka Kawahito Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
description	Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite involved in many critical cellular processes, including proliferation, migration, and angiogenesis, through interaction with a family of five G protein-coupled receptors (S1P1-5). Some reports have implicated S1P as an important inflammatory mediator of the pathogenesis of airway inflammation, but the role of S1P3 in the pathogenesis of lung diseases is not completely understood. We used S1P3-deficient (knockout (KO)) mice to clarify the role of S1P3 receptor signaling in the pathogenesis of pulmonary inflammation and fibrosis using a bleomycin-induced model of lung injury. On the seventh day after bleomycin administration, S1P3 KO mice exhibited significantly less body weight loss and pulmonary inflammation than wild-type (WT) mice. On the 28th day, there was less pulmonary fibrosis in S1P3 KO mice than in WT mice. S1P3 KO mice demonstrated a 56% reduction in total cell count in bronchoalveolar lavage fluid (BALF) collected on the seventh day compared with WT mice; however, the differential white blood cell profiles were similar. BALF analysis on the seventh day showed that connective tissue growth factor (CTGF) levels were significantly decreased in S1P3 KO mice compared with WT mice, although no differences were observed in monocyte chemotactic protein-1 (MCP-1) or transforming growth factor β1 (TGF-β1) levels. Finally, S1P levels in BALF collected on the 7th day after treatment were not significantly different between WT and S1P3 KO mice. Our results indicate that S1P3 receptor signaling plays an important role in pulmonary inflammation and fibrosis and that this signaling occurs via CTGF expression. This suggests that this pathway might be a therapeutic target for pulmonary fibrosis.
format	article
author	Ken Murakami Masataka Kohno Masatoshi Kadoya Hidetake Nagahara Wataru Fujii Takahiro Seno Aihiro Yamamoto Ryo Oda Hiroyoshi Fujiwara Toshikazu Kubo Satoshi Morita Hiroshi Nakada Timothy Hla Yutaka Kawahito
author_facet	Ken Murakami Masataka Kohno Masatoshi Kadoya Hidetake Nagahara Wataru Fujii Takahiro Seno Aihiro Yamamoto Ryo Oda Hiroyoshi Fujiwara Toshikazu Kubo Satoshi Morita Hiroshi Nakada Timothy Hla Yutaka Kawahito
author_sort	Ken Murakami
title	Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
title_short	Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
title_full	Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
title_fullStr	Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
title_full_unstemmed	Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
title_sort	knock out of s1p3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/172555b6a02d4e149684be58e8f01622
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Knock out of S1P3 receptor signaling attenuates inflammation and fibrosis in bleomycin-induced lung injury mice model.

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