Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786950 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17161176_subreads.fastq.gz | Fastqsanger.gz |
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Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating 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 Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.
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Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating 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 Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.
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Project description:Metabolic diseases, such as obesity, diabetes, and cardiovascular diseases, pose significant health challenges in contemporary society. The development of these diseases is closely related to the balance of gut microbiota, the functionality of metabolic products, and metabolic dysregulation across various tissues and organs. Tibetan tea, a traditional post-fermented tea originating from Ya'an, Sichuan in Southwest China, is known for its unique fermentation process and flavor, as well as its multitude of health benefits, such as acting as a prebiotic, antioxidant, blood sugar reducer, antithrombotic, and obesity prevention agent. This has sparked widespread interest among scholars both domestically and internationally in its potential to address metabolic diseases such as obesity, diabetes, hyperlipidemia, and thrombosis formation. However, current research has mostly focused on the effects on single tissues, with less exploration into the role of Tibetan tea in multi-tissue responses. Therefore, this study employed large-scale sequencing technologies to deeply analyze the impact of Tibetan tea extract intervention on the gut microbiota and peripheral blood, as well as on the metabolism of 10 different tissues and organs, including the brain, brown fat, heart, liver, kidneys, pancreas, colon, white fat, skeletal muscle, and bone marrow in C57BL/6J mice under both normal and high-fat diet conditions. The aim was to reveal the holistic response and mechanism of host metabolism to Tibetan tea intervention, thereby providing new insights into nutritional intervention strategies for metabolic diseases.
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