ArticleAdipocyte2021
POU2AF1 promotes MSCs adipogenesis by inhibiting HDAC1 expression.
Article in Adipocyte, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Subtype-specific dependencies and therapeutic opportunities in small cell lung cancer.Science advances · 2026Review
- Exploring Monogenic, Polygenic, and Epigenetic Models of Common Variable Immunodeficiency.Human mutation · 2025Review
- HDAC1 disrupts the tricarboxylic acid (TCA) cycle through the deacetylation of Nur77 and promotes inflammation in ischemia-reperfusion mice.Cell death discovery · 2023Article
- POU Class 2 Associating Factor 1 Exerts a Protective Effect on the Respiratory Syncytial Virus-Induced Acute Bronchiolitis by the NF-Evidence-based complementary and alternative medicine : eCAM · 2023Article
- The vulnerable primed cancer stem cells in disguise: demystifying the role of Maspin.Cancer metastasis reviews · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive production of visceral adipose is a major risk factor of many diseases. Inhibiting the adipogenesis of mesenchymal stem cells (MSCs) will be an efficient way to block adipose production. We illuminated POU class 2 homeobox associating factor 1 (POU2AF1) may promote MSCs adipogenesis by histone deacetylases 1 (HDAC1) signalling. Human retroperitoneal adipose-derived mesenchymal stem cells were isolated from overweight and control groups of patients. IncRNA microarray was used to identified gene expression levels. Adenovirus transduction and cellular small-interfering RNA transfection were used to achieve overexpression and interference of POU2AF1 or HDAC1. Adipogenesis was identified by Oil-red O staining, triglycende, cholesterol assay, real-time PCR and Western Blot. POU2AF1 expression was upregulated in retroperitoneal adipose tissue of overweight patients, and increased during adipogenesis. Overexpression of POU2AF1 promoted spontaneous adipogenesis without adipogenic treatment. Silencing of endogenous POU2AF1 in MSCs inhibited adipogenesis. Overexpression of POU2AF1 alleviated the translocation of HDAC1 to the nucleus. The mRNA level of HDAC1 was also reduced. Co-transfection of Ad-POU2AF1 and Ad-HDAC1 partially reversed the promotion effect of POU2AF1 overexpression in MSCs spontaneous adipogenic differentiation. POU2AF1 involves in the natural differentiation of human mesenchymal stem cells. Overexpression or silencing POU2AF1 could effectively induce or inhibit the adipogenesis by HDAC1 signaling.
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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.