ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Adipocyte expression of PU.1 transcription factor causes insulin resistance through upregulation of inflammatory cytokine gene expression and ROS production.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review.Frontiers in endocrinology · 2021Pooled it
- Significantly altered peripheral blood cell DNA methylation profile as a result of immediate effect of metformin use in healthy individuals.Clinical epigenetics · 2018Trial
- Role of the E26 transformation specific transcription factor family in metabolic disorders.Journal of endocrinological investigation · 2025Review
- Article
- Shared pathogenic mechanisms linking obesity and idiopathic pulmonary fibrosis revealed by bioinformatics and in vivo validation.Scientific reports · 2025Article
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- Development and validation of a predictive model for severe white matter hyperintensity with obesity.Frontiers in aging neuroscience · 2024Article
- Nutraceutical Prevention of Diabetic Complications-Focus on Dicarbonyl and Oxidative Stress.Current issues in molecular biology · 2022Review
- Benefits of Valsartan and Amlodipine in Lipolysis through PU.1 Inhibition in Fructose-Induced Adiposity.Nutrients · 2022Article
- Ainsliadimer C, a disesquiterpenoid isolated from Ainsliaea macrocephala, ameliorates inflammatory responses in adipose tissue via Sirtuin 1-NLRP3 inflammasome axis.Acta pharmacologica Sinica · 2022Article
- A nine-hub-gene signature of metabolic syndrome identified using machine learning algorithms and integrated bioinformatics.Bioengineered · 2021Article
- Implications of metabolism-driven myeloid dysfunctions in cancer therapy.Cellular & molecular immunology · 2021Review
- Adipocyte-Specific Ablation of PU.1 Promotes Energy Expenditure and Ameliorates Metabolic Syndrome in Aging Mice.Frontiers in aging · 2021Article
- Small molecule-driven SIRT3-autophagy-mediated NLRP3 inflammasome inhibition ameliorates inflammatory crosstalk between macrophages and adipocytes.British journal of pharmacology · 2020Article
- Effects of spirulina on weight loss and blood lipids: a review.Open heart · 2020Review
- SIRT3 promotes lipophagy and chaperon-mediated autophagy to protect hepatocytes against lipotoxicity.Cell death and differentiation · 2020Article
- Adipocyte PU.1 knockout promotes insulin sensitivity in HFD-fed obese mice.Scientific reports · 2019Article
- Myricanol modulates skeletal muscle-adipose tissue crosstalk to alleviate high-fat diet-induced obesity and insulin resistance.British journal of pharmacology · 2019Article
- Estradiol and NADPH oxidase crosstalk regulates responses to high fat feeding in female mice.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
We have reported previously that ETS family transcription factor PU.1 is expressed in mature adipocytes of white adipose tissue. PU.1 expression is increased greatly in mouse models of genetic or diet-induced obesity. Here, we show that PU.1 expression is increased only in visceral but not subcutaneous adipose tissues of obese mice, and the adipocytes are responsible for this increase in PU.1 expression. To further address PU.1's physiological function in mature adipocytes, PU.1 was knocked down in 3T3-L1 cells using retroviral-mediated expression of PU.1-targeting shRNA. Consistent with previous findings that PU.1 regulates its target genes, such as NADPH oxidase subunits and proinflammatory cytokines in myeloid cells, the mRNA levels of proinflammatory cytokines (TNFα, IL-1β, and IL-6) and cytosolic components of NADPH oxidase (p47phox and p40phox) were downregulated significantly in PU.1-silenced adipocytes. NADPH oxidase is a main source for reactive oxygen species (ROS) generation. Indeed, silencing PU.1 suppressed NADPH oxidase activity and attenuated ROS in basal or hydrogen peroxide-treated adipocytes. Silencing PU.1 in adipocytes suppressed JNK1 activation and IRS-1 phosphorylation at Ser(307). Consequently, PU.1 knockdown improved insulin signaling and increased glucose uptake in basal and insulin-stimulated conditions. Furthermore, knocking down PU.1 suppressed basal lipolysis but activated stimulated lipolysis. Collectively, these findings indicate that obesity induces PU.1 expression in adipocytes to upregulate the production of ROS and proinflammatory cytokines, both of which lead to JNK1 activation, insulin resistance, and dysregulation of lipolysis. Therefore, PU.1 might be a mediator for obesity-induced adipose inflammation and insulin resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.