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Dysbacteriosis‐induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling
Author(s) -
Song Jinhuan,
Wang Chaojie,
Long Denglu,
Li Ziguang,
You Lingsen,
BrandSaberi Beate,
Wang Guang,
Yang Xuesong
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201902965r
Subject(s) - myogenesis , retinoic acid , somitogenesis , biology , microbiology and biotechnology , progenitor cell , gut flora , dysbiosis , immunology , myocyte , stem cell , somite , genetics , embryogenesis , gene , embryo
Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, first we show the elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Second, we demonstrate that the diameter of muscle fibers, limb development, and somitogenesis were inhibited in both the gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and key genes which regulate the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS‐induced reactive oxygen species (ROS generation and antioxidant genes such as Nrf2, AKR1B10) contributed to the above ‐mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis is also involved in regulating the development of muscle progenitor cells during pregnancy.