GADD45α drives brown adipose tissue formation through upregulating PPARγ in mice

Xu, Zhonglin; Sun, Ye; Valencak, Teresa G.; Wang, Yizhen; Shan, Tizhong

doi:10.1038/s41419-020-02802-5

Cited by 13 publications

(26 citation statements)

References 65 publications

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“…Given that mitochondrial remodeling is required for the differentiation of myoblasts into myotubes and that GADD45B may affect mitochondria biogenesis in brown adipocytes, [28][29][30] we sought to determine whether GADD45B plays a role in mitochondria biogenesis during myogenic differentiation. Transmission electron microscopy was used to detect the status of mitochondrial networks in differentiating cells.…”

Section: Gadd45b Affects Myogenic Differentiation and Myoblast Mitochondria Biogenesismentioning

confidence: 99%

FTO-mediated demethylation of GADD45B promotes myogenesis through the activation of p38 MAPK pathway

Deng

Fan

Liang

et al. 2021

Molecular Therapy - Nucleic Acids

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N6-methyladenosine (m 6 A) modification plays a critical role in mammalian development. However, the role of m 6 A in the skeletal muscle development remains largely unknown. Here, we report a global m 6 A modification pattern of goat skeletal muscle at two key development stages and identified that the m 6 A modification regulated the expression of the growth arrest and DNA damage-inducible 45B (GADD45B) gene, which is involved in myogenic differentiation. We showed that GADD45B expression increased during myoblast differentiation, whereas the downregulation of GADD45B inhibits myogenic differentiation and mitochondrial biogenesis. Moreover, the expression of GADD45B regulates the expression of myogenic regulatory factors and peroxisome proliferatoractivated receptor gamma coactivator 1 alpha by activating the p38 mitogen-activated protein kinase (MAPK) pathway. Conversely, the inactivation of p38 MAPK abolished the GADD45B-mediated myogenic differentiation. Furthermore, we found that the knockdown of fat mass and obesity-associated protein (FTO) increases GADD45B m 6 A modification and decreases the stability of GADD45B mRNA, which impairs myogenic differentiation. Our results indicate that the FTOmediated m 6 A modification in GADD45B mRNA drives skeletal muscle differentiation by activating the p38 MAPK pathway, which provides a molecular mechanism for the regulation of myogenesis via RNA methylation.

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Section: Gadd45b Affects Myogenic Differentiation and Myoblast Mitochondria Biogenesismentioning

confidence: 99%

FTO-mediated demethylation of GADD45B promotes myogenesis through the activation of p38 MAPK pathway

Deng

Fan

Liang

et al. 2021

Molecular Therapy - Nucleic Acids

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“…GADD45A is a stress response protein related to DNA repair, the cell cycle, apoptosis, angiogenesis, and DNA demethylation [ 36 – 43 ]. PPARγ and GADD45A can pull each other down and colocalize in cells, indicating that GADD45A may regulate the transcriptional activities of PPARγ [ 44 ]. Furthermore, PPARγ2, an isoform of PPARγ, bound the CXCL3 promoter to regulate CXCL3 expression [ 45 – 47 ].…”

Section: Discussionmentioning

confidence: 99%

The long noncoding RNA TARID regulates the CXCL3/ERK/MAPK pathway in trophoblasts and is associated with preeclampsia

Liao

Liu

Gao

et al. 2022

Reprod Biol Endocrinol

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Background The widely accepted explanation of preeclampsia (PE) pathogenesis is insufficient trophoblast invasion and impaired uterine spiral artery remodeling. However, the underlying molecular mechanism remains unclear. Methods We performed transcriptome sequencing on placentas of normal and PE patients and identified 976 differentially expressed long noncoding RNAs (lncRNAs). TCF21 antisense RNA inducing demethylation (TARID) was one of the most significantly differentially expressed lncRNAs and was negatively correlated with the systolic and diastolic blood pressure in PE patients. Furthermore, we verified the effect of TARID on the biological behavior of trophoblasts and performed UID mRNA-seq to identify the effectors downstream of TARID. Then, co-transfection experiments were used to better illustrate the interaction between TARID and its downstream effector. Results We concluded that the downregulation of TARID expression may inhibit trophoblast infiltration and spiral artery remodeling through inhibition of cell migration, invasion, and tube formation mediated through the CXCL3/ERK/MAPK pathway. Conclusions Overall, these findings suggested that TARID may be a therapeutic target for PE through the CXCL3/ERK/MAPK pathway.

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“…The GTT and ITT were performed as described by You et al . (2020). At week 8, for GTT, mice were injected intraperitoneally with 400 mg ml ‐1 of D‐glucose (2 g kg ‐1 body weight; Aladdin, Shanghai, China) after 12 h fasting, and their blood glucose was measured by glucometer (Yuwell, Jiangsu, China) at 0, 15, 30, 60, 90, 120 min post‐injection respectively.…”

Section: Methodsmentioning

confidence: 99%

Faecal microbiota transplantation‐mediated jejunal microbiota changes halt high‐fat diet‐induced obesity in mice via retarding intestinal fat absorption

Zhu

Xiao

et al. 2021

Microbial Biotechnology

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Summary Faecal Microbiota Transplantation (FMT) is considered as a promising technology to fight against obesity. Wild boar has leanermuscle and less fat in comparison to the domestic pig, which were thought to be related with microbiota. To investigate the function and mechanism of the wild boar microbiota on obesity, we first analysed the wild boar microbiota composition via 16S rDNA sequencing, which showed that Firmicutes and Proteobacteria were the dominant bacteria. Then, we established a high‐fat diet (HFD)‐induced obesity model, and transfer low and high concentrations of wild boar faecal suspension in mice for 9 weeks. The results showed that FMT prevented HFD‐induced obesity and lipid metabolism disorders, and altered the jejunal microbiota composition especially increasing the abundance of the Lactobacillus and Romboutsia, which were negatively correlated with obesity‐related indicators. Moreover, we found that the anti‐obesity effect of wild boar faecal suspension was associated with jejunal N6‐methyladenosine (m6A) levels. Overall, these results suggest that FMT has a mitigating effect on HFD‐induced obesity, which may be due to the impressive effects of FMT on the microbial composition and structure of the jejunum. These changes further alter intestinal lipid metabolism and m6A levels to achieve resistance to obesity.

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GADD45α drives brown adipose tissue formation through upregulating PPARγ in mice

Cited by 13 publications

References 65 publications

FTO-mediated demethylation of GADD45B promotes myogenesis through the activation of p38 MAPK pathway

FTO-mediated demethylation of GADD45B promotes myogenesis through the activation of p38 MAPK pathway

The long noncoding RNA TARID regulates the CXCL3/ERK/MAPK pathway in trophoblasts and is associated with preeclampsia

Faecal microbiota transplantation‐mediated jejunal microbiota changes halt high‐fat diet‐induced obesity in mice via retarding intestinal fat absorption

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