Next Article in Journal
Efficacy of Bee Venom Acupuncture for Chronic Low Back Pain: A Randomized, Double-Blinded, Sham-Controlled Trial
Previous Article in Journal
The Unexpected Tuners: Are LncRNAs Regulating Host Translation during Infections?
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Toxins 2017, 9(11), 359;

TGF-β1/Smad3 Signaling Pathway Mediates T-2 Toxin-Induced Decrease of Type II Collagen in Cultured Rat Chondrocytes

Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention/ Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health (23618504), Harbin Medical University, Harbin 150081, China
Institute of Cell Biotechnology, China and Russia Medical Research Center, Harbin Medical University, Harbin 150081, China
Gaoqiao Community Health Service Center of Pudong New District, Shanghai 200137, China
Author to whom correspondence should be addressed.
Academic Editors: James J. Pestka and Marc Maresca
Received: 6 July 2017 / Revised: 8 August 2017 / Accepted: 2 November 2017 / Published: 5 November 2017
(This article belongs to the Section Mycotoxins)
Full-Text   |   PDF [2958 KB, uploaded 7 November 2017]   |  


T-2 toxin can cause damage to the articular cartilage, but the molecular mechanism remains unclear. By employing the culture of rat chondrocytes, we investigated the effect of the TGF-β1/Smad3 signaling pathway on the damage to chondrocytes induced by T-2 toxin. It was found that T-2 toxin could reduce cell viability and increased the number of apoptotic cells when compared with the control group. After the addition of the T-2 toxin, the production of type II collagen was reduced at mRNA and protein levels, while the levels of TGF-β1, Smad3, ALK5, and MMP13 were upregulated. The production of the P-Smad3 protein was also increased. Inhibitors of TGF-β1 and Smad3 were able to reverse the effect of the T-2 toxin on the protein level of above-mentioned signaling molecules. The T-2 toxin could promote the level of MMP13 via the stimulation of TGF-β1 signaling in chondrocytes, resulting in the downregulation of type II collagen and chondrocyte damage. Smad3 may be involved in the degradation of type II collagen, but the Smad3 has no connection with the regulation of MMP13 level. This study provides a new clue to elucidate the mechanism of T-2 toxin-induced chondrocyte damage. View Full-Text
Keywords: T-2 toxin; chondrocytes; TGF-β1; Smad3; type II collagen T-2 toxin; chondrocytes; TGF-β1; Smad3; type II collagen

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Li, Y.; Zou, N.; Wang, J.; Wang, K.-W.; Li, F.-Y.; Chen, F.-X.; Sun, B.-Y.; Sun, D.-J. TGF-β1/Smad3 Signaling Pathway Mediates T-2 Toxin-Induced Decrease of Type II Collagen in Cultured Rat Chondrocytes. Toxins 2017, 9, 359.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Toxins EISSN 2072-6651 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top