Mouse microRNA-124 regulates the expression of Hes1 in P19 cells
Open accessAbstract
MicroRNAs (miRNAs) belong to a conserved class of small non-coding RNAs that are typically 18-25 nucleotides long. They are found in both animals and plants. These small RNAs can regulate gene expression at translational level by interacting with their target messenger RNAs, and they play an essential role in the development of plants and animals. To date, more than 200 miRNAs have been identified in mammals; however, their mRNA targets have not yet been identified. In this study, we demonstrate that the expression of Hes-1, which is a basic helix-loop-helix transcriptional repressor, is regulated by miRNA-124 in P19 cells. Reduction in the levels of miR-124 mediated by locked nucleic acids resulted in the accumulation of Hes-1 and hindered the retinoic acid-induced neuronal differentiation of P19 cells. Thus, our results indicate that miR-124 regulates the expression of Hes-1 at the post-transcriptional level and is involved in the retinoic acid-induced neuronal differentiation of P19 cells.
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Hes1 is an authentic target of miR-23.
“A basic helix-loop-helix transcriptional repressor, named Hes1, is an authentic target of miR-23.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
Section 4.3 identifies Hes-1 as a target of miR-124 in P19 cells, not miR-23. The Discussion likewise attributes the observed regulation of Hes-1 protein to miR-124. The cited paper therefore supports a different microRNA identity than the one attributed to it. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredDecrease in miR-23 levels can lead to accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.
“The decrease in miR-23 levels can lead to the accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
The Abstract reports that reducing miR-124 caused Hes-1 to accumulate and hindered retinoic-acid-induced neuronal differentiation in P19 cells. The claim instead names miR-23 and NT2 cells, neither of which is supported by that passage. (LLM, conf=0.88)
Experimental — accuracy not yet measuredHes1 is also directly targeted by miR-124, and knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.
“Hes1 is also directly targeted by miR-124, and the knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
Section 4.2 reports that locked nucleic acids reduced miR-124 in differentiated P19 cells and increased Hes-1 protein; section 4.3 identifies partial sequence complementarity and says Hes-1 may be a miR-124 target. The paper does not establish direct targeting definitively, and it does not compare the effect with miR-23 inhibition. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredExpression level of Hes1 increases, ultimately hindering neuronal differentiation of P19 cells induced by retinoic acid.
“The expression level of Hes1 increases, ultimately hindering neuronal differentiation of P19 cells induced by the retinoic acid [[129], [130], [131]].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
The Abstract reports that reducing miR-124 with locked nucleic acids caused Hes-1 to accumulate and hindered retinoic-acid-induced neuronal differentiation of P19 cells. The claim omits that experimental condition: Results §4.1 instead reports that Hes-1 was barely detectable after differentiation, so an unqualified increase during differentiation is not supported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRegulation of neural development by miR-23 is probably achieved through the combined action of other miRNAs.
“It indicates that the regulation of neural development by miR-23 is probably achieved through the combined action of other miRNAs.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
The Introduction says several miRNAs may collaborate in regulating neuronal differentiation. But the paper studies miR-124, not miR-23, and does not establish that miR-23 acts with other miRNAs in neural development. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
miR-23 is specifically expressed in astrocytes of the adult brain and is one of the miRNAs highly expressed in neurons during brain development.
“miR-23 is specifically expressed in astrocytes of the adult brain and is one of the miRNAs that are highly expressed in neurons during brain development.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
The Introduction (page unavailable) discusses brain-expressed miRNAs induced during P19-cell differentiation, but does not identify miR-23 among them. Searches for miR-23, adult-brain astrocytes, and neuronal expression during brain development found no passage addressing the claim; the Discussion instead concerns miR-124. (LLM, conf=0.75)
Experimental — accuracy not yet measuredmiR-23 has the ability to affect neural differentiation.
“miR-23 has the ability to affect neural differentiation.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [131]
The Results (section 4.1) and Discussion (section 5) address miR-124 and neural differentiation in P19 cells, not miR-23. A search of our copy for miR-23 found no passage addressing whether it affects neural differentiation; the miR-124 finding does not establish or refute the claim about miR-23. Page numbers were not provided. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Ma, X.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Corresponding author
- Ma, Xu
- ORCID
- Ma, Xu
- Venue
- Frontiers in Bioscience
- Publisher
- IMR Press
- Published
- 2010
- Volume
- E2
- Issue
- 1
- Pages
- 127-132
- ISSN
- 1944-7892 (ISSN-L)
- 1945-0494
- 1945-0508
- DOI
- 10.2741/e74
- OpenAlex
- W2330522727
- Cited by
- 21
- References
- 26
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 2 · 2020: 1 · 2019: 2 · 2016: 2 · 2014: 4 · 2013: 2 · 2012: 4
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Frontiers in Bioscience-Elite (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Key Research and Development Program of China (2007CB5119005)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- miR-124, Hes1, P19 cells, neuronal differentiation, retinoic acid, post-transcriptional regulation, locked nucleic acid, microRNA target regulation
- MeSH terms
- Transcription Factor HES-1, Animals, Cell Differentiation, Gene Expression Regulation, Tretinoin, Blotting, Western, DNA Primers, Homeodomain Proteins, Reverse Transcriptase Polymerase Chain Reaction, MicroRNAs, Cell Line, Tumor, Mice, Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Proteins
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