Tags

Type your tag names separated by a space and hit enter

Elevation of IGFBP2 contributes to mycotoxin T-2-induced chondrocyte injury and metabolism.
Biochem Biophys Res Commun. 2016 09 09; 478(1):385-391.BB

Abstract

Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy. The mycotoxin of T-2 toxin is extensively accepted as a major etiological contributor to KBD. However, its function and mechanism in KBD remains unclearly elucidated. Here, T-2 toxin treatment induced chondrocyte injury in a time- and dose-dependent manner by repressing cell viability and promoting cell necrosis and apoptosis. Importantly, T-2 suppressed the transcription of type II collagen and aggrecan, as well as the release of sulphated glycosaminoglycan (sGAG). Furthermore, exposure to T-2 enhanced the transcription of matrix metalloproteinases (MMPs), including MMP-1, -2, -3 and -9. In contrast to control groups, higher expression of insulin-like growth factor binding protein 2 (IGFBP2) was observed in chondrocytes from KBD patients. Interestingly, T-2 toxin caused a dramatical elevation of IGFBP2 expression in chondrocytes. Mechanism analysis corroborated that cessation of IGFBP2 expression alleviated T-2-induced damage to chondrocytes. Simultaneously, transfection with IGFBP2 siRNA also attenuated matrix synthesis and catabolism-related gene expressions of MMPs. Together, this study validated that T-2 toxin exposure might promote the progression of KBD by inducing chondrocyte injury, suppressing matrix synthesis and accelerating cellular catabolism through IGFBP2. Therefore, this research will elucidate a new insight about how T-2 toxin participate in the pathogenesis of KBD.

Authors+Show Affiliations

Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.Department of Endocrinology, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, 76 West Yanta Road, Xi'an, Shaanxi 710061, PR China. Electronic address: xiongguoxa@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27416762

Citation

Wang, Xiaoqing, et al. "Elevation of IGFBP2 Contributes to Mycotoxin T-2-induced Chondrocyte Injury and Metabolism." Biochemical and Biophysical Research Communications, vol. 478, no. 1, 2016, pp. 385-391.
Wang X, Zhang Y, Chang Y, et al. Elevation of IGFBP2 contributes to mycotoxin T-2-induced chondrocyte injury and metabolism. Biochem Biophys Res Commun. 2016;478(1):385-391.
Wang, X., Zhang, Y., Chang, Y., Duan, D., Sun, Z., & Guo, X. (2016). Elevation of IGFBP2 contributes to mycotoxin T-2-induced chondrocyte injury and metabolism. Biochemical and Biophysical Research Communications, 478(1), 385-391. https://doi.org/10.1016/j.bbrc.2016.07.042
Wang X, et al. Elevation of IGFBP2 Contributes to Mycotoxin T-2-induced Chondrocyte Injury and Metabolism. Biochem Biophys Res Commun. 2016 09 9;478(1):385-391. PubMed PMID: 27416762.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Elevation of IGFBP2 contributes to mycotoxin T-2-induced chondrocyte injury and metabolism. AU - Wang,Xiaoqing, AU - Zhang,Yan, AU - Chang,Yanhai, AU - Duan,Dapeng, AU - Sun,Zhengming, AU - Guo,Xiong, Y1 - 2016/07/11/ PY - 2016/06/19/received PY - 2016/07/08/accepted PY - 2016/7/16/entrez PY - 2016/7/16/pubmed PY - 2017/5/24/medline KW - Chondrocyte injury KW - Chondrocyte metabolism KW - IGFBP2 KW - Kashin-Beck disease KW - Mycotoxin T-2 SP - 385 EP - 391 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 478 IS - 1 N2 - Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy. The mycotoxin of T-2 toxin is extensively accepted as a major etiological contributor to KBD. However, its function and mechanism in KBD remains unclearly elucidated. Here, T-2 toxin treatment induced chondrocyte injury in a time- and dose-dependent manner by repressing cell viability and promoting cell necrosis and apoptosis. Importantly, T-2 suppressed the transcription of type II collagen and aggrecan, as well as the release of sulphated glycosaminoglycan (sGAG). Furthermore, exposure to T-2 enhanced the transcription of matrix metalloproteinases (MMPs), including MMP-1, -2, -3 and -9. In contrast to control groups, higher expression of insulin-like growth factor binding protein 2 (IGFBP2) was observed in chondrocytes from KBD patients. Interestingly, T-2 toxin caused a dramatical elevation of IGFBP2 expression in chondrocytes. Mechanism analysis corroborated that cessation of IGFBP2 expression alleviated T-2-induced damage to chondrocytes. Simultaneously, transfection with IGFBP2 siRNA also attenuated matrix synthesis and catabolism-related gene expressions of MMPs. Together, this study validated that T-2 toxin exposure might promote the progression of KBD by inducing chondrocyte injury, suppressing matrix synthesis and accelerating cellular catabolism through IGFBP2. Therefore, this research will elucidate a new insight about how T-2 toxin participate in the pathogenesis of KBD. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/27416762/Elevation_of_IGFBP2_contributes_to_mycotoxin_T_2_induced_chondrocyte_injury_and_metabolism_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(16)31157-3 DB - PRIME DP - Unbound Medicine ER -