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Published on: September 14, 2021
TGF-β1/Smad3 Signaling Pathway Mediates T-2 Toxin-Induced Decrease of Type II Collagen in Cultured Rat Chondrocytes
Yang Li1, Ning Zou2, Jing Wang3
1Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China. yangli9295@hotmail.com.
Abstract:
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.
Insights
T-2 toxin damages articular cartilage by upregulating the TGF-β1/Smad3 pathway, increasing MMP13, and reducing type II collagen. This leads to chondrocyte apoptosis and cartilage damage.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- T-2 toxin is known to cause articular cartilage damage.
- The precise molecular mechanisms underlying T-2 toxin-induced chondrocyte damage are not fully understood.
Purpose of the Study:
- To investigate the role of the transforming growth factor-beta 1 (TGF-β1)/Smad3 signaling pathway in T-2 toxin-induced chondrocyte damage.
- To elucidate the molecular mechanisms of T-2 toxin's effects on articular cartilage.
Main Methods:
- Primary rat chondrocytes were cultured and treated with T-2 toxin.
- Cell viability and apoptosis were assessed.
- Levels of type II collagen, TGF-β1, Smad3, ALK5, and matrix metalloproteinase 13 (MMP13) were measured at mRNA and protein levels.
- Inhibitors of TGF-β1 and Smad3 were used to explore pathway involvement.
Main Results:
- T-2 toxin reduced chondrocyte viability and increased apoptosis.
- T-2 toxin decreased type II collagen production while upregulating TGF-β1, Smad3, ALK5, and MMP13.
- Increased phosphorylation of Smad3 (P-Smad3) was observed.
- TGF-β1 and Smad3 inhibitors partially reversed T-2 toxin's effects.
- T-2 toxin promotes MMP13 via TGF-β1 signaling, leading to collagen II downregulation and chondrocyte damage.
Conclusions:
- The TGF-β1/Smad3 signaling pathway is implicated in T-2 toxin-induced chondrocyte damage.
- T-2 toxin-induced MMP13 upregulation contributes to type II collagen reduction and chondrocyte injury.
- Smad3 may play a role in type II collagen degradation, independent of MMP13 regulation.
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