ArticleInternational journal of obesity (2005)2015
Mesoderm-specific transcript (MEST) is a negative regulator of human adipocyte differentiation.
Article in International journal of obesity (2005), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
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- Dissecting Heterogeneity Reveals a Unique BAMBIAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Mouse mesoderm-specific transcript inhibits adipogenic differentiation and induces trans-differentiation into hepatocyte-like cells in 3T3-L1 preadiocytes.BMC research notes · 2022Article
- Characterization of transcript enrichment and detection bias in single-nucleus RNA-seq for mapping of distinct human adipocyte lineages.Genome research · 2022Article
- Metabolomic profiles and microbiota of GDM offspring: The key for future perspective?Frontiers in pediatrics · 2022Review
- Induced pluripotent stem cell-derived smooth muscle cells to study cardiovascular calcification.Frontiers in cardiovascular medicine · 2022Article
- Long non-coding RNA NEAT1 facilitates the growth, migration, and invasion of ovarian cancer cells via the let-7 g/MEST/ATGL axis.Cancer cell international · 2021Article
- Chemically Defined Xeno- and Serum-Free Cell Culture Medium to Grow Human Adipose Stem Cells.Cells · 2021Article
- MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT.Translational cancer research · 2020Article
- ZFP57 suppress proliferation of breast cancer cells through down-regulation of MEST-mediated Wnt/β-catenin signalling pathway.Cell death & disease · 2019Article
- Candidate genes linking maternal nutrient exposure to offspring health via DNA methylation: a review of existing evidence in humans with specific focus on one-carbon metabolism.International journal of epidemiology · 2018Review
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- DNA methylation of imprinted genes at birth is associated with child weight status at birth, 1 year, and 3 years.Clinical epigenetics · 2018Article
- WISP1/CCN4 inhibits adipocyte differentiation through repression of PPARγ activity.Scientific reports · 2017Article
- Diet-induced adipose tissue expansion is mitigated in mice with a targeted inactivation of mesoderm specific transcript (Mest).PloS one · 2017Article
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundA growing body of evidence suggests that many downstream pathologies of obesity are amplified or even initiated by molecular changes within the white adipose tissue (WAT). Such changes are the result of an excessive expansion of individual white adipocytes and could potentially be ameliorated via an increase in de novo adipocyte recruitment (adipogenesis). Mesoderm-specific transcript (MEST) is a protein with a putative yet unidentified enzymatic function and has previously been shown to correlate with adiposity and adipocyte size in mouse.
objectivesThis study analysed WAT samples and employed a cell model of adipogenesis to characterise MEST expression and function in human. METHODS AND
resultsMEST mRNA and protein levels increased during adipocyte differentiation of human multipotent adipose-derived stem cells. Further, obese individuals displayed significantly higher MEST levels in WAT compared with normal-weight subjects, and MEST was significantly correlated with adipocyte volume. In striking contrast to previous mouse studies, knockdown of MEST enhanced human adipocyte differentiation, most likely via a significant promotion of peroxisome proliferator-activated receptor signalling, glycolysis and fatty acid biosynthesis pathways at early stages. Correspondingly, overexpression of MEST impaired adipogenesis. We further found that silencing of MEST fully substitutes for the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) as an inducer of adipogenesis. Accordingly, phosphorylation of the pro-adipogenic transcription factors cyclic AMP responsive element binding protein (CREB) and activating transcription factor 1 (ATF1) were highly increased on MEST knockdown.
conclusionsAlthough we found a similar association between MEST and adiposity as previously described for mouse, our functional analyses suggest that MEST acts as an inhibitor of human adipogenesis, contrary to previous murine studies. We have further established a novel link between MEST and CREB/ATF1 that could be of general relevance in regulation of metabolism, in particular obesity-associated diseases.
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