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The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis

BACKGROUND: This study aimed to investigate the effect of abnormal Core binding factor-β expression on proliferation, differentiation and apoptosis of chondrocytes, and elucidate the relationship between Core binding factor-β and osteoarthritis-related markers and degenerative joint disease. METHODS...

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Autores principales: Li, Guangdi, Zhang, Mi, Huang, Yuan, Yang, Jiafei, Dong, Lianghong, Shi, Hao, Li, Long, Liu, Riguang, Li, Jiangwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879671/
https://www.ncbi.nlm.nih.gov/pubmed/33573620
http://dx.doi.org/10.1186/s12891-021-04043-9
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author Li, Guangdi
Zhang, Mi
Huang, Yuan
Yang, Jiafei
Dong, Lianghong
Shi, Hao
Li, Long
Liu, Riguang
Li, Jiangwei
author_facet Li, Guangdi
Zhang, Mi
Huang, Yuan
Yang, Jiafei
Dong, Lianghong
Shi, Hao
Li, Long
Liu, Riguang
Li, Jiangwei
author_sort Li, Guangdi
collection PubMed
description BACKGROUND: This study aimed to investigate the effect of abnormal Core binding factor-β expression on proliferation, differentiation and apoptosis of chondrocytes, and elucidate the relationship between Core binding factor-β and osteoarthritis-related markers and degenerative joint disease. METHODS: Cartilage tissues, from healthy subjects and patients with osteoarthritis, were collected for histology and expression of Core binding factor-β, MMP-13, IL-1β, COMP, and YKL-40. Human articular chondrocytes were cultured in vitro, and a viral vector was constructed to regulate cellular Core binding factor-β expression. Cellular proliferation and apoptosis were observed, and osteoarthritis-related inflammatory factor expression and cartilage metabolite synthesis assayed. RESULTS: Human osteoarthritis lesions had disordered cartilage structure and cellular arrangement, and increased emptying of cartilage lacunae. Normal cell counts were significantly reduced, cartilage extracellular matrix was obviously damaged, and type II collagen expression was significantly decreased. Core binding factor-β was highly expressed in the osteoarthritis cartilage (p < 0.001), and MMP-13, IL-1β, COMP and YKL-40 expression were greater than found in normal cartilage (p < 0.001). Cellular proliferation in the Core binding factor-β high-expression group was reduced and the total apoptosis rate was increased (p < 0.05), while the opposite was found in the Core binding factor-β inhibition group (p < 0.01). Compared with normal chondrocytes, high Core binding factor-β expression (Osteoarthritis and CBFB/pCDH groups) was associated with significantly increased MMP13, IL-1β, COMP and YKL-40 protein expression (p < 0.01), while Core binding factor-β inhibition (CBFB/pLKO.1 group) was associated with significantly decreased COMP, MMP13, IL-1β and YKL-40 expression in osteoarthritis cells (p < 0.001). CONCLUSIONS: Abnormal Core binding factor-β expression might play an upstream regulatory role in mediating abnormal chondrocyte apoptosis and the inflammatory response. On inhibiting Core binding factor-β expression, a delay in cartilage degeneration was expected. TRIAL REGISTRATION: The study was registered for clinical trials in ChiCTR: ChiCTR1800017066 (Reg. Date-2018/7/10).
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spelling pubmed-78796712021-02-17 The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis Li, Guangdi Zhang, Mi Huang, Yuan Yang, Jiafei Dong, Lianghong Shi, Hao Li, Long Liu, Riguang Li, Jiangwei BMC Musculoskelet Disord Research Article BACKGROUND: This study aimed to investigate the effect of abnormal Core binding factor-β expression on proliferation, differentiation and apoptosis of chondrocytes, and elucidate the relationship between Core binding factor-β and osteoarthritis-related markers and degenerative joint disease. METHODS: Cartilage tissues, from healthy subjects and patients with osteoarthritis, were collected for histology and expression of Core binding factor-β, MMP-13, IL-1β, COMP, and YKL-40. Human articular chondrocytes were cultured in vitro, and a viral vector was constructed to regulate cellular Core binding factor-β expression. Cellular proliferation and apoptosis were observed, and osteoarthritis-related inflammatory factor expression and cartilage metabolite synthesis assayed. RESULTS: Human osteoarthritis lesions had disordered cartilage structure and cellular arrangement, and increased emptying of cartilage lacunae. Normal cell counts were significantly reduced, cartilage extracellular matrix was obviously damaged, and type II collagen expression was significantly decreased. Core binding factor-β was highly expressed in the osteoarthritis cartilage (p < 0.001), and MMP-13, IL-1β, COMP and YKL-40 expression were greater than found in normal cartilage (p < 0.001). Cellular proliferation in the Core binding factor-β high-expression group was reduced and the total apoptosis rate was increased (p < 0.05), while the opposite was found in the Core binding factor-β inhibition group (p < 0.01). Compared with normal chondrocytes, high Core binding factor-β expression (Osteoarthritis and CBFB/pCDH groups) was associated with significantly increased MMP13, IL-1β, COMP and YKL-40 protein expression (p < 0.01), while Core binding factor-β inhibition (CBFB/pLKO.1 group) was associated with significantly decreased COMP, MMP13, IL-1β and YKL-40 expression in osteoarthritis cells (p < 0.001). CONCLUSIONS: Abnormal Core binding factor-β expression might play an upstream regulatory role in mediating abnormal chondrocyte apoptosis and the inflammatory response. On inhibiting Core binding factor-β expression, a delay in cartilage degeneration was expected. TRIAL REGISTRATION: The study was registered for clinical trials in ChiCTR: ChiCTR1800017066 (Reg. Date-2018/7/10). BioMed Central 2021-02-11 /pmc/articles/PMC7879671/ /pubmed/33573620 http://dx.doi.org/10.1186/s12891-021-04043-9 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Li, Guangdi
Zhang, Mi
Huang, Yuan
Yang, Jiafei
Dong, Lianghong
Shi, Hao
Li, Long
Liu, Riguang
Li, Jiangwei
The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title_full The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title_fullStr The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title_full_unstemmed The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title_short The relationship between abnormal Core binding factor-β expression in human cartilage and osteoarthritis
title_sort relationship between abnormal core binding factor-β expression in human cartilage and osteoarthritis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879671/
https://www.ncbi.nlm.nih.gov/pubmed/33573620
http://dx.doi.org/10.1186/s12891-021-04043-9
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