The Journal of endocrinology
April 21, 2026 · via Europe PMC
The impact and potential mechanisms of long noncoding RNA ENST00000521141.1 on human white adipocyte differentiation.
Wu Q, You L, Lin S, +5 more, Pang L.
AI summary — for doctors, generated from the abstract only
Knocking down the long noncoding RNA ENST00000521141.1 suppressed human preadipocyte differentiation, apparently through upregulation of PDGFRA.
What was studied
A cell study using microarray screening, knockdown and overexpression, FISH localization, RNA sequencing, and rescue experiments in human preadipocytes.
Key findings
- lncRNA521141 was enriched in differentiated adipocytes and localized mainly to the nucleus
- Knockdown reduced lipid accumulation, triglyceride content, and adipogenic markers; overexpression had no effect
- PI3K-Akt and thyroid hormone synthesis pathways were implicated
- PDGFRA was upregulated after knockdown, and its knockdown reversed the inhibition of differentiation
Clinical relevance
Identifies a possible molecular target for obesity research; findings are in cell culture.
Who should care
Limitations
In vitro human cell study only.
A nuclear long noncoding RNA helps drive human fat cell development.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Accumulation of visceral white adipose tissue leads to central obesity and is associated with insulin resistance and increased risk of metabolic disease. lncRNAs have been reported to regulate the growth and development of adipocytes, providing new clues for the prevention and treatment of obesity. In the present study, we identified numerous dysregulated lncRNAs by microarray analysis between human differentiated adipocytes and preadipocytes. In addition, we focused on the lncRNA ENST00000521141.1 (abbreviated as lncRNA521141) confirmed by qRT-PCR to be enriched in differentiated adipocytes. Lentivirus-mediated knockdown of lncRNA521141 significantly suppressed adipogenesis as evidenced by reduced lipid accumulation, triglyceride content, and key adipogenic markers expression, while lentivirus-mediated lncRNA521141 overexpression showed no significant effect. Given that lncRNA521141 did not alter the expression of the neighboring gene PEBP4, fluorescence in situ hybridization was employed to elucidate the cellular localization of lncRNA521141, revealing its predominant distribution in the nucleus. RNA-sequencing and western blot analysis further revealed the potential involvement of the PI3K-Akt and thyroid hormone synthesis pathways in lncRNA521141-mediated adipogenic inhibition. Among the differentially expressed genes, PDGFRA expression was significantly upregulated following lncRNA521141 silencing and was closely associated with adipocyte differentiation. Rescue experiments confirmed that knockdown of PDGFRA expression after lncRNA521141 silencing alleviated the inhibitory effects of the reduced lncRNA521141 expression on adipocyte differentiation. In summary, the present study identified lncRNA521141 as a key regulator of adipogenic differentiation in human preadipocytes and elucidated its potential regulatory mechanism, thereby providing new insights and potential intervention targets for treating obesity and its related diseases.
DOI
10.1530/joe-25-0360
PMID
41944396
PMCID
PMC13130826
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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