Role of the high-affinity leukotriene B4 receptor signaling in fibrosis after unilateral ureteral obstruction in mice.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 05 08 2018
accepted: 10 02 2019
entrez: 1 3 2019
pubmed: 1 3 2019
medline: 4 12 2019
Statut: epublish

Résumé

Leukotriene B4 (LTB4) is a lipid mediator that acts as a potent chemoattractant for inflammatory leukocytes. Kidney fibrosis is caused by migrating inflammatory cells and kidney-resident cells. Here, we examined the role of the high-affinity LTB4 receptor BLT1 during development of kidney fibrosis induced by unilateral ureteral obstruction (UUO) in wild-type (WT) mice and BLT1 knockout (BLT1-/-) mice. We found elevated expression of 5-lipoxygenase (5-LOX), which generates LTB4, in the renal tubules of UUO kidneys from WT mice and BLT1-/- mice. Accumulation of immunoreactive type I collagen in WT UUO kidneys increased over time; however, the increase was less prominent in BLT1-/- UUO kidneys. Accumulation of S100A4-positive fibroblasts increased temporally in WT UUO kidneys, but was again less pronounced in-BLT1-/- UUO kidneys. The same was true of mRNA encoding transforming growth factor-β (TGF)-β and fibroblast growth factor (FGF)-2. Finally, accumulation of F4/80-positive macrophages, which secrete TGF-β, increased temporally in WT UUO and BLT1-/- UUO kidneys, but to a lesser extent in the latter. Following LTB4 stimulation in vitro, macrophages showed increased expression of mRNA encoding TGF-β/FGF-2 and Col1a1, whereas L929 fibroblasts showed increased expression of mRNA encoding α smooth muscle actin (SMA). Bone marrow (BM) transplantation studies revealed that the area positive for type I collagen was significantly smaller in BLT1-/-BM→WT than in WT-BM→WT. Thus, LTB4-BLT1 signaling plays a critical role in fibrosis in UUO kidneys by increasing accumulation of macrophages and fibroblasts. Therefore, blocking BLT1 may prevent renal fibrosis.

Identifiants

pubmed: 30818366
doi: 10.1371/journal.pone.0202842
pii: PONE-D-18-23121
pmc: PMC6394974
doi:

Substances chimiques

Ltb4r1 protein, mouse 0
Receptors, Leukotriene B4 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0202842

Commentaires et corrections

Type : ErratumIn

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Mariko Kamata (M)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
Department of Nephrology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.

Hideki Amano (H)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, Kanagawa, Japan.

Yoshiya Ito (Y)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, Kanagawa, Japan.

Tomoe Fujita (T)

Department of Pharmacology and Toxicology, Dokkyo Medical University, Shimotsuga-gun, Tochigi, Japan.

Fumisato Otaka (F)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.

Kanako Hosono (K)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, Kanagawa, Japan.

Kouju Kamata (K)

Sagamiono Medical and Kidney Clinic, Sagamihara Kanagawa, Japan.

Yasuo Takeuchi (Y)

Department of Nephrology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.

Takehiko Yokomizo (T)

Department of Biochemistry, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.

Takao Shimizu (T)

Department of Lipidomics, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Department of Lipid Signaling, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.

Masataka Majima (M)

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara Kanagawa, Japan.
Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, Kanagawa, Japan.

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Classifications MeSH