MyD88 deficiency ameliorates weight loss caused by intestinal oxidative injury in an autophagy‐dependent mechanism

Background Gut health plays a vital role in the overall health and disease control of human and animals. Intestinal oxidative stress is a critical player in the induction and progression of cachexia which is conventionally diagnosed and classified by weight loss. Therefore, reduction of intestinal o...

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Published in:Journal of cachexia, sarcopenia and muscle sarcopenia and muscle, 2022-02, Vol.13 (1), p.677-695
Main Authors: Qi, Ming, Liao, Simeng, Wang, Jing, Deng, Yuankun, Zha, Andong, Shao, Yirui, Cui, Zhijuan, Song, Tongxing, Tang, Yulong, Tan, Bie, Yin, Yulong
Format: Article
Language:English
Subjects:
Animals
Antibodies
Apoptosis
Autophagy
Cachexia
Cell cycle
Cell growth
CRISPR
DNA damage repair
Homeostasis
Intestinal epithelial cells
Mice
Mitochondrial fission
Myeloid Differentiation Factor 88 - genetics
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Original : Basic Science
Oxidative Stress
Paraquat - pharmacology
Penicillin
Primary Immunodeficiency Diseases
Proteins
Reactive oxygen species
Weight Loss
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Summary:Background Gut health plays a vital role in the overall health and disease control of human and animals. Intestinal oxidative stress is a critical player in the induction and progression of cachexia which is conventionally diagnosed and classified by weight loss. Therefore, reduction of intestinal oxidative injury is a common and highly effective strategy for the maintenance of human and animal health. Here we identify intestinal myeloid differentiation primary response gene 88 (MyD88) as a novel target for intestinal oxidative stress using canonical oxidative stress model induced by paraquat (PQ) in vitro and in vivo. Methods Intestinal oxidative stress was induced by administration of PQ in intestinal epithelial cells (IECs) and mouse model. Cell proliferation, apoptosis, DNA damage, mitochondrial function, oxidative status, and autophagy process were measured in wild‐type and MyD88‐deficient IECs during PQ exposure. Autophagy inhibitor (3‐methyladenine) and activator (rapamycin) were employed to assess the role of autophagy in MyD88‐deficient IECs during PQ exposure. MyD88 specific inhibitor, ST2825, was used to verify function of MyD88 during PQ exposure in mouse model. Results MyD88 protein levels and apoptotic rate of IECs are increased in response to PQ exposure (P 
ISSN:2190-5991
2190-6009
DOI:10.1002/jcsm.12858