Leukemia inhibitory factor shortens primary cilia by upregulating C-C motif chemokine 2 in human neural stem/progenitor cells.


Journal

Genes to cells : devoted to molecular & cellular mechanisms
ISSN: 1365-2443
Titre abrégé: Genes Cells
Pays: England
ID NLM: 9607379

Informations de publication

Date de publication:
Dec 2023
Historique:
revised: 03 10 2023
received: 31 05 2023
accepted: 03 10 2023
medline: 4 12 2023
pubmed: 15 10 2023
entrez: 14 10 2023
Statut: ppublish

Résumé

Primary cilia on neural stem/progenitor cells (NSPCs) play an important role in determining cell fate, although the regulatory mechanisms involved in the ciliogenesis remain largely unknown. In this study, we analyzed the effect of the leukemia inhibitory factor (LIF) for the primary cilia in immortalized human NSPCs. LIF withdrawal elongated the primary cilia length, whereas the addition of LIF shortened it. Microarray gene expression analysis revealed that differentially expressed genes (DEGs) associated with LIF treatment were related with the multiple cytokine signaling pathways. Among the DEGs, C-C motif chemokine 2 (CCL2) had the highest ranking and its increase in the protein concentration in the NSPCs-conditioned medium after the LIF treatment was confirmed by ELISA. Interestingly, we found that CCL2 was a negative regulator of cilium length, and LIF-induced shortening of primary cilia was antagonized by CCL2-specific antibody, suggesting that LIF could influence cilia length via upregulating CCL2. The shortening effect of LIF and CCL2 on primary cilia was also observed in SH-SY5Y cells. The results of the study suggested that the LIF-CCL2 axis may well be a regulator of NSPCs and its primary cilia length, which could affect multiple cellular processes, including NSPC proliferation and differentiation.

Identifiants

pubmed: 37837427
doi: 10.1111/gtc.13074
doi:

Substances chimiques

Leukemia Inhibitory Factor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

868-880

Subventions

Organisme : JSPS-KAKENHI, Grants-in-Aid for Scientific Research
ID : 21H02883

Informations de copyright

© 2023 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd.

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Auteurs

Hisashi Takahashi (H)

Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.

Takahiro Fujimoto (T)

Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.

Takeshi Yaoi (T)

Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.

Shinji Fushiki (S)

Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.

Kyoko Itoh (K)

Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.

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