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Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis.
Sci Rep. 2020 Apr 22; 10(1):6824.SR

Abstract

The pathological mechanism of Kashin-Beck disease (KBD), an endemic osteoarthritic disease, remains to be poorly understood. This study was designed to identify signaling pathways and crucial proteins involved in the pathological mechanism of KBD compared with osteoarthritis (OA). The knee cartilage samples were collected from gender- and age-matched KBD (n = 9) and OA (n = 9) patients. After pre-processing, samples were labeled with Tamdem Mass Tags 6plex multiplex kit, and analyzed by liquid chromatography-tandem mass spectrometry. Proteomic results were analyzed with gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interactions (PPI). The differential abundance proteins from KBD and OA were validated using western blot analysis. As a result, A total number of 375 proteins were identified to have differential abundance between KBD and OA, of which 121 and 254 proteins were observed to be up-regulated or down-regulated in KBD group. GO analysis shows that the differential abundant proteins are associated with cell junction and signal transducer activity from extracellular to intracellular. KEGG pathways enrichment and PPI network indicate four major pathways, including extracellular matrix -receptor interaction, focal adhesion, phosphatidylinositol 3-kinase (PI3K)-Protein kinase B (Akt), and Ras signaling pathways were involved in the degeneration of cartilage. Moreover, integrins, laminins, NF-κB and other regulative molecules were found as crucial proteins. In conclusion, our results demonstrated that compared with OA, the differential abundance proteins and signaling pathways may contribute to the occurrence and development of joint damage in KBD. Further investigation of their regulative roles and interaction may provide new insights into the pathological mechanisms and therapeutic targets for KBD.

Authors+Show Affiliations

School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China. Shenzhen Institute, Xi'an Jiaotong University, Shenzhen, Guangdong, 518057, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China. Shenzhen Institute, Xi'an Jiaotong University, Shenzhen, Guangdong, 518057, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China.Laboratory of Resource Biology and Biotechnology in Western China (Ministry of Education), Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest University, Xi'an, Shaanxi, 710069, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China. bbbishop@126.com. Shenzhen Institute, Xi'an Jiaotong University, Shenzhen, Guangdong, 518057, P. R. China. bbbishop@126.com.School of Public Health, Health Science Center; Key Laboratory of Environment and Gene Related Diseases of Ministry Education; Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, P. R. China. Department of Integrative Medical Biology, Umeå University, Umeå, 90187, Sweden.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32322000

Citation

Lei, Jian, et al. "Proteomic Analysis of Knee Cartilage Reveals Potential Signaling Pathways in Pathological Mechanism of Kashin-Beck Disease Compared With Osteoarthritis." Scientific Reports, vol. 10, no. 1, 2020, p. 6824.
Lei J, Amhare AF, Wang L, et al. Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis. Sci Rep. 2020;10(1):6824.
Lei, J., Amhare, A. F., Wang, L., Lv, Y., Deng, H., Gao, H., Guo, X., Han, J., & Lammi, M. J. (2020). Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis. Scientific Reports, 10(1), 6824. https://doi.org/10.1038/s41598-020-63932-6
Lei J, et al. Proteomic Analysis of Knee Cartilage Reveals Potential Signaling Pathways in Pathological Mechanism of Kashin-Beck Disease Compared With Osteoarthritis. Sci Rep. 2020 Apr 22;10(1):6824. PubMed PMID: 32322000.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis. AU - Lei,Jian, AU - Amhare,Abebe Feyissa, AU - Wang,Liyun, AU - Lv,Yizhen, AU - Deng,Huan, AU - Gao,Hang, AU - Guo,Xiong, AU - Han,Jing, AU - Lammi,Mikko J, Y1 - 2020/04/22/ PY - 2019/09/15/received PY - 2020/04/03/accepted PY - 2020/4/24/entrez PY - 2020/4/24/pubmed PY - 2020/4/24/medline SP - 6824 EP - 6824 JF - Scientific reports JO - Sci Rep VL - 10 IS - 1 N2 - The pathological mechanism of Kashin-Beck disease (KBD), an endemic osteoarthritic disease, remains to be poorly understood. This study was designed to identify signaling pathways and crucial proteins involved in the pathological mechanism of KBD compared with osteoarthritis (OA). The knee cartilage samples were collected from gender- and age-matched KBD (n = 9) and OA (n = 9) patients. After pre-processing, samples were labeled with Tamdem Mass Tags 6plex multiplex kit, and analyzed by liquid chromatography-tandem mass spectrometry. Proteomic results were analyzed with gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interactions (PPI). The differential abundance proteins from KBD and OA were validated using western blot analysis. As a result, A total number of 375 proteins were identified to have differential abundance between KBD and OA, of which 121 and 254 proteins were observed to be up-regulated or down-regulated in KBD group. GO analysis shows that the differential abundant proteins are associated with cell junction and signal transducer activity from extracellular to intracellular. KEGG pathways enrichment and PPI network indicate four major pathways, including extracellular matrix -receptor interaction, focal adhesion, phosphatidylinositol 3-kinase (PI3K)-Protein kinase B (Akt), and Ras signaling pathways were involved in the degeneration of cartilage. Moreover, integrins, laminins, NF-κB and other regulative molecules were found as crucial proteins. In conclusion, our results demonstrated that compared with OA, the differential abundance proteins and signaling pathways may contribute to the occurrence and development of joint damage in KBD. Further investigation of their regulative roles and interaction may provide new insights into the pathological mechanisms and therapeutic targets for KBD. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/32322000/Proteomic_analysis_of_knee_cartilage_reveals_potential_signaling_pathways_in_pathological_mechanism_of_Kashin-Beck_disease_compared_with_osteoarthritis L2 - http://dx.doi.org/10.1038/s41598-020-63932-6 DB - PRIME DP - Unbound Medicine ER -
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