ArticleMetabolism: clinical and experimental2019
Inflammation and ER stress differentially regulate STAMP2 expression and localization in adipocytes.
Article in Metabolism: clinical and experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Excessive or sustained endoplasmic reticulum stress: one of the culprits of adipocyte dysfunction in obesity.Therapeutic advances in endocrinology and metabolism · 2024Review
- 4-PBA inhibits hypoxia-induced lipolysis in rat adipose tissue and lipid accumulation in the liver through regulating ER stress.Food science & nutrition · 2023Article
- Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats.Frontiers in pharmacology · 2023Article
- The Role of Adipocyte Endoplasmic Reticulum Stress in Obese Adipose Tissue Dysfunction: A Review.International journal of general medicine · 2023Review
- Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology.Frontiers in endocrinology · 2022Review
- STAMP2 suppresses autophagy in prostate cancer cells by modulating the integrated stress response pathway.American journal of cancer research · 2022Article
- PERK signaling pathway in bone metabolism: Friend or foe?Cell proliferation · 2021Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundChronic ER stress and dysfunction is a hallmark of obesity and a critical contributor to metaflammation, abnormal hormone action and altered substrate metabolism in metabolic tissues, such as liver and adipocytes. Lack of STAMP2 in lean mice induces inflammation and insulin resistance on a regular diet, and it is dysregulated in the adipose tissue of obese mice and humans. We hypothesized that the regulation of STAMP2 is disrupted by ER stress.
methods3T3-L1 and MEF adipocytes were treated with ER stress inducers thapsigargin and tunicamycin, and inflammation inducer TNFα. The treatments effect on STAMP2 expression and enzymatic function was assessed. In addition, 3T3-L1 adipocytes and HEK cells were utilized for Stamp2 promoter activity investigation performed with luciferase and ChIP assays.
resultsER stress significantly reduced both STAMP2 mRNA and protein expression in cultured adipocytes whereas TNFα had the opposite effect. Concomitant with loss of STAMP2 expression during ER stress, intracellular localization of STAMP2 was altered and total iron reductase activity was reduced. Stamp2 promoter analysis by reporter assays and chromatin immunoprecipitation, showed that induction of ER stress disrupts C/EBPα-mediated STAMP2 expression.
conclusionThese data suggest a clear link between ER stress and quantitative and functional STAMP2-deficiency.
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