Slug transcription factor and nuclear Lamin B1 are upregulated in osteoarthritic chondrocytes

Osteoarthritis and Cartilage
Roberta PivaGina Lisignoli

Abstract

To contribute to clarify molecular mechanisms supporting senescence and de-differentiation of chondrocytes in chondrocyte pathologies such as osteoarthritis (OA). Specifically, we investigated the relationship between the nuclear lamina protein Lamin B1 and the negative regulator of chondrogenesis Slug transcription factor in osteoarthritic chondrocytes. Lamin B1 and Slug proteins were analyzed in cartilage explants from normal subjects and OA patients by immunohistochemical technique. Their expression was confirmed on isolated chondrocytes both at passage 0 and passage 2 (de-differentiated chondrocytes) by immunofluorescence and western blot. Subsequently, we explored the "in vivo" binding of Slug on LMNB1 promoter by chromatin immunoprecipitation assay (ChIP). In this study we demonstrated that nuclear lamina protein Lamin B1 and anti-chondrogenic Slug transcription factor are upregulated in cartilage and OA chondrocytes. Furthermore, we found that Slug is "in vivo" recruited by LMNB1 gene promoter mostly when chondrocytes undergo de-differentiation or OA degeneration. We described for the first time a potential regulatory role of Slug on the LMNB1 gene expression in OA chondrocytes. These findings may have important implicat...Continue Reading

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Citations

Oct 30, 2016·Seminars in Cell & Developmental Biology·Chia-Feng LiuVéronique Lefebvre
Sep 4, 2018·Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society·Andrea LolliGerjo J V M van Osch
Jun 25, 2021·Frontiers in Cell and Developmental Biology·Chao YangQiang Chen

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