| Literature DB >> 33578291 |
Shu-Ming Chen1, Ali Raza Jahejo1, Fazul Nabi2, Shakeel Ahmed3, Jin-Feng Zhao1, Jin Yu1, Chen-Liang Zhang1, Guan-Bao Ning1, Ding Zhang1, Sayed Haidar Abbas Raza4, Wen-Xia Tian5.
Abstract
Pathogenicity of tibial dyschondroplasia (TD) in broiler chickens is not detected yet. Janus Kinase/Signal Transducer and Activator of Transcription (JAK-STAT) signaling pathway-related genes were investigated in thiram induced TD chickens. Real-time qPCR and immunohistochemical (IHC) technique were used to observe the expression changes of STAT3 and SOSC3 gene on days 1, 2, 4, 6 after feeding 100 mg·kg-1 thiram. Morphological, pathological, and histological results of this study suggested that chondrocyte cells were observed more damaged on day 6 than day 1, 2, and 4. Therefore, Lameness and damaged chondrocytes gradually increased from day 1 to 6. The mRNA expression level of STAT3 was observed insignificant (P > 0.05) in thiram induced TD chickens' group of day 1. However, on days 2, 4, and 6, the expression was significant (P < 0.05). SOCS3 increased in thiram group on days 1, 2 and 6, decreased on day 4 (P < 0.05). The p-STAT3 and SOCS3 protein's protein localization was evaluated in the control and thiram-induced TD broiler chickens through IHC, suggesting that SOSC3 protein was observed significantly higher on days 1, 2, and 6 and down-regulated on day 4. p-STAT3 protein on thiram induced group was observed significantly upregulated on days 4 and 6. In conclusion, the differential expression of STAT3 and SOCS3 showed that the JAK-STAT signaling pathway might play an important role in regulating an abnormal proliferation, differentiation, or apoptosis of chondrocytes in TD at an early stage.Entities:
Keywords: Chicken; Chondrocytes; Growth plate; JAK/STAT; SOCS3; p-STAT3
Year: 2021 PMID: 33578291 DOI: 10.1016/j.rvsc.2021.01.024
Source DB: PubMed Journal: Res Vet Sci ISSN: 0034-5288 Impact factor: 2.534