Stomatin modulates adipogenesis through the ERK pathway and regulates fatty acid uptake and lipid droplet growth

Wu, Shao-Chin; Lo, Yuan-Ming; Lee, Jui-Hao; Chen, Chin-Yau; Chen, Tung-Wei; Liu, Hong‐Wen; Lian, Wei-Nan; Hua, Kate; Liao, Chi Chang; Lin, Win-Li; Yang, Chih‐Yung; Tung, Chien-Yi; Lin, Chi-Hung

doi:10.1038/s41467-022-31825-z

Cited by 17 publications

(11 citation statements)

References 75 publications

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“…Even so, in accordance with in vitro research with contradicting findings, it was found that sustained adipogenesis would decrease if ERK was activated because peroxisome proliferator-activated receptor (PPAR)γ expression can be inhibited by prolonged stimulation of the sustained activation through MAPK40-mediated phosphorylation [33] .…”

Section: Resultsmentioning

confidence: 67%

The anti-obesity properties of Anredera cordifolia leaf extract in rats fed a high-fat diet through inhibition of adipogenesis

Rusdiana,

Widyawati,

Sari

et al. 2024

J Adv Vet Anim Res

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Objective: Various disease complications are a risk of overweight or obesity, so losing weight can reduce the risk of diseases caused by obesity. Binahong leaf ethanol extract (Anredera cordifolia) is a weight-loss herbal preparation. Aim: This study aims to analyze whether A. cordifolia extract is effective in losing weight by affecting the mechanism of adipogenesis in an animal obesity model. Materials and Methods: Animals were grouped into six groups as follows: the normal diet (K1), the negative control group (K2), the positive control group with Orlistat at a dose of 20 mg/kg BW (K3), an ethanol extract of A. cordifolia leaves at doses of 50 mg/kg BW (P1), 100 mg/kg BW group (P2), and 150 mg/kg BW (P3). All rats were fed a diet that consisted of high fat for eight weeks, except K1. Afterward, the treatments were given based on group distribution. Then, the rats were treated based on their groups for 4 weeks, and the high-fat diet was still given during the treatment for the control groups (K2). Anthropometric examinations such as body weight, length, and the circumference of the abdomen were measured. Metabolic parameters, including blood glucose, cholesterol levels, triglyceride levels, and abdominal fat weight, were measured using molecular parameters that measured PI3K levels and Extracellular signal-regulated kinase (ERK) in abdominal fat tissue samples using the ELISA method. Results: ERK levels of abdominal fat were lowered in the treatment group using the extract of A. cordifolia (50 mg/kg BW (P1) and 100 mg/kg BW (P2)) compared to the control group that was given a high-fat diet without treatment. The control group, which was fed a high-fat diet without treatment, had an average ERK level of 10.17 ± 2.98 ng/ml, P1 (50 mg/kg BW). Furthermore, when ethanol extracts were used as opposed to the control group, which received a high-fat diet without treatment, there was an increase in phosphoinositide three-kinase (PI3K) levels (K2). The control group received 9.35 ± 2.87 ng/ml, the treatment group received 100 mg/kg BW (P2) 9.48 ± 1.54 ng/ml, and the treatment group received 150 mg/kg BW (P3) 7.87 ± 1.79 ng/ml. The weight of fat in the abdomen differed between the groups that received a high-fat diet without treatment (K2) and those that received a high-fat diet with treatment (P1, P2, P3; p < 0.05). Conclusion: Anredera cordifolia extract possesses anti-obesity activities by decreasing ERK and increasing PI3K levels, as well as reducing abdominal fat weight.

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Section: Resultsmentioning

confidence: 67%

The anti-obesity properties of Anredera cordifolia leaf extract in rats fed a high-fat diet through inhibition of adipogenesis

Rusdiana,

Widyawati,

Sari

et al. 2024

J Adv Vet Anim Res

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“…Similarly, Wu et al. found that inhibiting the STOM gene increased ERK1/2 phosphorylation while reducing PPARγ expression and lipid accumulation in 3T3‐L1 cells 42 . Liu et al.…”

Section: Discussionmentioning

confidence: 93%

“…41 Similarly, Wu et al found that inhibiting the STOM gene increased ERK1/2 phosphorylation while reducing PPARγ expression and lipid accumulation in 3T3-L1 cells. 42 Liu et al discovered that F I G U R E 6 Exploring the mechanism of CPM-regulated BMSC differentiation. (A) Principal component analysis (PCA) shows transcriptome heterogeneity of BMSCs between the CPM knockdown group (siCPM) and control group (siNC).…”

Section: Discussionmentioning

confidence: 99%

Carboxypeptidase M modulates BMSCs osteogenesis–adipogenesis via the MAPK/ERK pathway: An integrated single‐cell and bulk transcriptomic study

Liao,

Zheng,

et al. 2024

The FASEB Journal

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The pathogenesis of osteoporosis (OP) is closely associated with the disrupted balance between osteogenesis and adipogenesis in bone marrow‐derived mesenchymal stem cells (BMSCs). We analyzed published single‐cell RNA sequencing (scRNA‐seq) data to dissect the transcriptomic profiles of bone marrow‐derived cells in OP, reviewing 56 377 cells across eight scRNA‐seq datasets from femoral heads (osteoporosis or osteopenia n = 5, osteoarthritis n = 3). Seventeen genes, including carboxypeptidase M (CPM), were identified as key osteogenesis‐adipogenesis regulators through comprehensive gene set enrichment, differential expression, regulon activity, and pseudotime analyses. In vitro, CPM knockdown reduced osteogenesis and promoted adipogenesis in BMSCs, while adenovirus‐mediated CPM overexpression had the reverse effects. In vivo, intraosseous injection of CPM‐overexpressing BMSCs mitigated bone loss in ovariectomized mice. Integrated scRNA‐seq and bulk RNA sequencing analyses provided insight into the MAPK/ERK pathway's role in the CPM‐mediated regulation of BMSC osteogenesis and adipogenesis; specifically, CPM overexpression enhanced MAPK/ERK signaling and osteogenesis. In contrast, the ERK1/2 inhibitor binimetinib negated the effects of CPM overexpression. Overall, our findings identify CPM as a pivotal regulator of BMSC differentiation, which provides new clues for the mechanistic study of OP.

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“…The lipid elevation concerns cholesterol rather than triglycerides, although the latter correlate positively with chemerin in metabolic disorders [ 33 , 34 ]. Both in vivo and in vitro studies have shown that chemerin promotes lipid uptake and storage, evidenced by the enhanced production of PPARg [ 35 ], adiponectin [ 36 ], p-ERK1/2 [ 37 – 39 ], and FABP4 [ 40 ]. In HTR-8/SVneo trophoblast cells, chemerin increased cholesterol biosynthesis by upregulating SREBP2 [ 41 ], while it diminished LDL endocytosis via downregulation of both the LDLR and SORT1 [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

Adipokine chemerin overexpression in trophoblasts leads to dyslipidemia in pregnant mice: implications for preeclampsia

et al. 2023

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Background The adipokine chemerin regulates adipogenesis and the metabolic function of both adipocytes and liver. Chemerin is elevated in preeclamptic women, and overexpression of chemerin in placental trophoblasts induces preeclampsia-like symptoms in mice. Preeclampsia is known to be accompanied by dyslipidemia, albeit via unknown mechanisms. Here, we hypothesized that chemerin might be a contributor to dyslipidemia. Methods Serum lipid fractions as well as lipid-related genes and proteins were determined in pregnant mice with chemerin overexpression in placental trophoblasts and chemerin-overexpressing human trophoblasts. In addition, a phospholipidomics analysis was performed in chemerin-overexpressing trophoblasts. Results Overexpression of chemerin in trophoblasts increased the circulating and placental levels of cholesterol rather than triglycerides. It also increased the serum levels of lysophosphatidic acid, high-density lipoprotein cholesterol (HDL-C), and and low-density lipoprotein cholesterol (LDL-C), and induced placental lipid accumulation. Mechanistically, chemerin upregulated the levels of peroxisome proliferator-activated receptor g, fatty acid-binding protein 4, adiponectin, sterol regulatory element-binding protein 1 and 2, and the ratio of phosphorylated extracellular signal-regulated protein kinase (ERK)1/2 / total ERK1/2 in the placenta of mice and human trophoblasts. Furthermore, chemerin overexpression in human trophoblasts increased the production of lysophospholipids and phospholipids, particularly lysophosphatidylethanolamine. Conclusions Overexpression of placental chemerin production disrupts trophoblast lipid metabolism, thereby potentially contributing to dyslipidemia in preeclampsia.

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Stomatin modulates adipogenesis through the ERK pathway and regulates fatty acid uptake and lipid droplet growth

Cited by 17 publications

References 75 publications

The anti-obesity properties of Anredera cordifolia leaf extract in rats fed a high-fat diet through inhibition of adipogenesis

The anti-obesity properties of Anredera cordifolia leaf extract in rats fed a high-fat diet through inhibition of adipogenesis

Carboxypeptidase M modulates BMSCs osteogenesis–adipogenesis via the MAPK/ERK pathway: An integrated single‐cell and bulk transcriptomic study

Adipokine chemerin overexpression in trophoblasts leads to dyslipidemia in pregnant mice: implications for preeclampsia

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