TRIM37 is highly expressed during mitosis in CHON-002 chondrocytes cell line and is regulated by miR-223
Autor: | Hakim Ouled-Haddou, Yohann Demont, Benjamin Brigant, Loïc Garçon, Sylvie Testelin, Valérie Metzinger-Le Meuth, Laurent Metzinger, Jacques Rochette |
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Přispěvatelé: | HEMATIM - Hématopoïèse et immunologie - UR UPJV 4666 (HEMATIM), Université de Picardie Jules Verne (UPJV)-CHU Amiens-Picardie-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Recherche Vasculaire Translationnelle (LVTS (UMR_S_1148 / U1148)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Université Sorbonne Paris Nord, CHU Amiens-Picardie, CHirurgie, IMagerie et REgénération tissulaire de l’extrémité céphalique - Caractérisation morphologique et fonctionnelle - UR UPJV 7516 (CHIMERE), Université de Picardie Jules Verne (UPJV) |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Mulibrey nanism Histology Physiology Endocrinology Diabetes and Metabolism [SDV]Life Sciences [q-bio] Ubiquitin-Protein Ligases Mitosis 030209 endocrinology & metabolism Biology Chondrocyte Cell Line Tripartite Motif Proteins 03 medical and health sciences 0302 clinical medicine Chondrocytes medicine Bone growth Cell growth Nuclear Proteins Cell cycle medicine.disease Chondrogenesis Cell biology MicroRNAs 030104 developmental biology medicine.anatomical_structure Cytoplasm |
Zdroj: | BONE BONE, Elsevier, 2020, 137, pp.115393-. ⟨10.1016/j.bone.2020.115393⟩ |
ISSN: | 1873-2763 8756-3282 |
DOI: | 10.1016/j.bone.2020.115393⟩ |
Popis: | Multiple molecular disorders can affect mechanisms regulating proliferation and differentiation of growth plate chondrocytes. Mutations in the TRIM37 gene cause the Mulibrey nanism, a heritable growth disorder. Since chondrocytes are instrumental in long bone growth that is deficient in nanism, we hypothesized that TRIM37 defect could contribute to dysregulation of the chondrocyte cell cycle. Western blotting, confocal microscopy and imaging flow cytometry determined TRIM37 expression in CHON-002 cell lineage. We showed that TRIM37 is expressed during mitosis of chondrocytes and directly impacted their proliferation. During the chondrocyte cell cycle, TRIM37 was present in both nucleus and cytoplasm. During M phase we observed an increase of the TRIM37-Tubulin co-localization in comparison with G1, S and G2 phases. TRIM37 knock down inhibited proliferation, together with cell cycle anomalies and increased autophagy, while overexpression accordingly enhanced cell proliferation. We demonstrated that microRNA-223 directly targets TRIM37, and suggest that miR-223 regulates TRIM37 gene expression during the cell cycle. In summary, our results give clues to explain why TRIM37 deficiency in chondrocytes impacts bone growth. Modulating TRIM37 using miR-223 could be an approach to increase chondrogenesis. |
Databáze: | OpenAIRE |
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