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Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes
This study aimed to investigate the expression of B‐cell lymphoma‐extra large (Bcl‐xL) in cartilage tissues following articular cartilage injury and to determine its effects on the biological function of chondrocytes. A total of 25 necrotic cartilage tissue samples and 25 normal tissue samples were...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7708954/ https://www.ncbi.nlm.nih.gov/pubmed/33304230 http://dx.doi.org/10.1002/elsc.202000039 |
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author | Pan, Zhengjun Yin, Hao Wang, Shuangli Xiong, Gaoxin Yin, Zongsheng |
author_facet | Pan, Zhengjun Yin, Hao Wang, Shuangli Xiong, Gaoxin Yin, Zongsheng |
author_sort | Pan, Zhengjun |
collection | PubMed |
description | This study aimed to investigate the expression of B‐cell lymphoma‐extra large (Bcl‐xL) in cartilage tissues following articular cartilage injury and to determine its effects on the biological function of chondrocytes. A total of 25 necrotic cartilage tissue samples and 25 normal tissue samples were collected from patients diagnosed with osteoarthritis at our hospital from December 2015 to December 2018. The mRNA expression levels of Bcl‐xL, caspase‐3, and matrix metalloproteinase‐3 (MMP‐3) in the normal and necrotic tissues were examined via quantitative polymerase chain reaction, and their protein expression levels were detected via western blotting. The expression levels of Bcl‐xL, insulin‐like growth factor‐1 (IGF‐1), and bone morphogenetic protein (BMP) were significantly lower but those of caspase‐3, MMP‐3, interleukin‐1β (IL‐1β), and chemokine‐like factor 1 (CKLF1) levels were markedly higher in necrotic cartilage tissues than in normal tissues. Following cell transfection, the expression levels of Bcl‐xL, IGF‐1, and BMP were remarkably higher but those of caspase‐3, MMP‐3, IL‐1β, and CKLF1 were notably lower in the Si‐Bcl‐xL group than in the NC group. The Si‐Bcl‐xL group showed significantly lower cell growth and noticeably higher apoptosis rate than the NC group (normal control group). The expression of Bcl‐xL is reduced following articular cartilage injury, and this reduction promotes the proliferation and inhibits the apoptosis of chondrocytes. Therefore, Bcl‐xL could serve as a relevant molecular target in the clinical practice of osteoarthritis and other diseases causing cartilage damage. |
format | Online Article Text |
id | pubmed-7708954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-77089542020-12-09 Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes Pan, Zhengjun Yin, Hao Wang, Shuangli Xiong, Gaoxin Yin, Zongsheng Eng Life Sci Research Articles This study aimed to investigate the expression of B‐cell lymphoma‐extra large (Bcl‐xL) in cartilage tissues following articular cartilage injury and to determine its effects on the biological function of chondrocytes. A total of 25 necrotic cartilage tissue samples and 25 normal tissue samples were collected from patients diagnosed with osteoarthritis at our hospital from December 2015 to December 2018. The mRNA expression levels of Bcl‐xL, caspase‐3, and matrix metalloproteinase‐3 (MMP‐3) in the normal and necrotic tissues were examined via quantitative polymerase chain reaction, and their protein expression levels were detected via western blotting. The expression levels of Bcl‐xL, insulin‐like growth factor‐1 (IGF‐1), and bone morphogenetic protein (BMP) were significantly lower but those of caspase‐3, MMP‐3, interleukin‐1β (IL‐1β), and chemokine‐like factor 1 (CKLF1) levels were markedly higher in necrotic cartilage tissues than in normal tissues. Following cell transfection, the expression levels of Bcl‐xL, IGF‐1, and BMP were remarkably higher but those of caspase‐3, MMP‐3, IL‐1β, and CKLF1 were notably lower in the Si‐Bcl‐xL group than in the NC group. The Si‐Bcl‐xL group showed significantly lower cell growth and noticeably higher apoptosis rate than the NC group (normal control group). The expression of Bcl‐xL is reduced following articular cartilage injury, and this reduction promotes the proliferation and inhibits the apoptosis of chondrocytes. Therefore, Bcl‐xL could serve as a relevant molecular target in the clinical practice of osteoarthritis and other diseases causing cartilage damage. John Wiley and Sons Inc. 2020-10-13 /pmc/articles/PMC7708954/ /pubmed/33304230 http://dx.doi.org/10.1002/elsc.202000039 Text en © 2020 The Authors. Engineering in Life Sciences published by Wiley‐VCH GmbH This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Pan, Zhengjun Yin, Hao Wang, Shuangli Xiong, Gaoxin Yin, Zongsheng Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title | Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title_full | Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title_fullStr | Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title_full_unstemmed | Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title_short | Bcl‐xL expression following articular cartilage injury and its effects on the biological function of chondrocytes |
title_sort | bcl‐xl expression following articular cartilage injury and its effects on the biological function of chondrocytes |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7708954/ https://www.ncbi.nlm.nih.gov/pubmed/33304230 http://dx.doi.org/10.1002/elsc.202000039 |
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