T-2 toxin-induced chondrocyte apoptosis contributes to growth plate damage through Smad2 and Smad3 signaling.
Toxicon
; 232: 107193, 2023 Aug 15.
Article
en En
| MEDLINE
| ID: mdl-37423522
ABSTRACT
The growth plate cartilage is one of the most common areas that Kashin-Beck Disease attacks. However, the exact mechanism of growth plate damage remains unclear. Here, we demonstrated that Smad2 and Smad3 were closely associated with the differentiation of chondrocytes. Reduction of Smad2 and Smad3 were found both in T-2 toxin-induced human chondrocytes in vitro and in T-2 toxin-induced rat growth plate in vivo. Blunting Smad2 or Smad3 both strikingly induced human chondrocytes apoptosis, implying a plausible signaling pathway to clarify the mechanism of T-2 toxin-induced oxidative damage. Furthermore, decreased Smad2 and Smad3 were also observed in the growth plates of KBD children. Collectively, our findings clearly illustrated that T-2 toxin-induced chondrocyte apoptosis contributes to growth plate damage through Smad2 and Smad3 signaling, which refines the pathogenesis of endemic osteoarthritis and provides two potential targets for the prevention and repairment of endemic osteoarthritis.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Osteoartritis
/
Toxina T-2
Límite:
Animals
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Child
/
Humans
Idioma:
En
Revista:
Toxicon
Año:
2023
Tipo del documento:
Article
País de afiliación:
Estados Unidos