Critical role of leukotriene B4 receptor signaling in mouse 3T3-L1 preadipocyte differentiation

• Published in: Lipids in health and disease 2013-08, Vol.12 (1), p.122-122, Article 122
• Main Authors: Hirata, Kae, Wada, Koichiro, Murata, Yuka, Nakajima, Atsushi, Yamashiro, Takashi, Kamisaki, Yoshinori
• Format: Article
• Language: English
• Subjects: 3T3-L1 Cells; Adipocytes; Adipocytes - drug effects; Adipocytes - metabolism; Analysis; Animals; Cell Differentiation - drug effects; Cell Differentiation - genetics; Cell growth; Control systems; Dentistry; Experiments; Health aspects; Insulin resistance; Insulin Resistance - genetics; Leukotriene B4 - genetics; Leukotriene B4 - metabolism; Leukotrienes; Lipids; Lipoxygenase - genetics; Lipoxygenase - metabolism; Lipoxygenase Inhibitors - administration & dosage; Mice; Obesity; Obesity - genetics; Obesity - metabolism; Obesity - pathology; Pharmaceutical industry; Proteins; Receptors, Leukotriene B4 - genetics; Receptors, Leukotriene B4 - metabolism; RNA, Small Interfering; Rodents; Signal Transduction - drug effects; Signal Transduction - genetics; Statistical analysis; Synthesis; Triglycerides
• ISSN: 1476-511X; 1476-511X
• DOI: 10.1186/1476-511x-12-122

Various inflammatory mediators related to obesity might be closely related to insulin resistance. Leukotrienes (LTs) are involved in inflammatory reactions. However, there are few reports regarding the role of LTs in adipocyte differentiation. Therefore, we investigated the role of leukotriene B4 (LTB4)-leukotriene receptor (BLT) signaling in mouse 3T3-L1 fibroblastic preadipocyte differentiation to mature adipocytes. Mouse 3T3-L1 preadipocytes were treated with lipoxygenase (LOX) inhibitors, BLT antagonist, and small interfering RNA (siRNA) for BLT1 and BLT2 to block the LTB4-BLT signaling pathway, then the adipocyte differentiation such as lipid accumulation and the increase in triglyceride was evaluated. Blockade of BLT signaling by treatment with a LOX inhibitor or a BLT antagonist suppressed preadipocyte differentiation into mature adipocytes. In addition, knockdown of BLT1 and BLT2 by siRNAs dramatically inhibited differentiation. These results indicate the LTB4-BLT signaling pathway may positively regulate preadipocyte differentiation and be a rate-limiting system to control adipocyte differentiation. The LTB4-BLT signaling pathway provides a potent regulatory signal that accelerates the differentiation of mouse 3T3-L1 preadipocytes. Further investigations are necessary to confirm the exact role of LTB4 and BLTs signaling pathways in preadipocyte differentiation.