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Screening of Proliferation-Related Genes and Pathological Changes in Thiram-Induced Tibial Dyschondroplasia.

Authors :
Jahejo, Ali Raza
Zhang, Chen-Liang
Nabi, Fazul
Kalhoro, Nazeer Hussain
Shah, Qurban Ali
Bhutto, Zohaib Ahmed
Zhao, Jin-Feng
Yu, Jin
Ning, Guan-Bao
Zhang, Ding
Chen, Shu-Ming
Tian, Wen-Xia
Source :
BioMed Research International; 7/14/2022, p1-9, 9p
Publication Year :
2022

Abstract

Aim and Background. Tibial dyschondroplasia (TD) is a tibiotarsal bone disorder of rapid growing poultry species. The complete pathogenicity of TD remains unknown; therefore, a study was conducted to screen possible role of proliferation-related gene expression in thiram-induced tibial TD chickens. Materials and Methods. Three hundred sixty (n = 360) broiler chickens were equally divided into control (C) and thiram (T) groups. Furthermore, the C and T groups were dividedinto 8-, 9-, 11-, and 13-day-old chickens. Results. Clinically, it was observed that broiler chickens of group T had abnormal posture, gait, and lameness, and histopathological results revealed dead and abnormal chondrocytes of T group on day 6. Real-time qPCR results showed that HDAC1, MTA1, H4, and PCNA genes were significantly expressed (P < 0.05). HDAC1 was upregulated on days 1, 2, 4, and 6 (P < 0.01); MTA1 was upregulated on days 1 and 2 (P < 0.01); H4 was upregulated on days 2 and 4 (P < 0.01), and PCNA was downregulated on days 1, 2, and 4 (P < 0.01). Furthermore, IHC results of HDAC1 protein were significantly (P < 0.01) expressed in proliferative zone of day 1 and hypertrophic zone of day 6. MTA1 protein was significantly (P < 0.01) expressed on days 1, 2, and 6 in all zones, except prehypertrophic zone of day 2. Conclusion. In conclusion, the mRNA expressions of HDAC1, MTA1, H4, and PCNA were differentially expressed in the chondrocytes of thiram-induced TD chickens. HDAC1 and MTA1 protein expression found involved and responsible in the abnormal chondrocytes' proliferation of broiler chicken. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
23146133
Database :
Complementary Index
Journal :
BioMed Research International
Publication Type :
Academic Journal
Accession number :
157989881
Full Text :
https://doi.org/10.1155/2022/6209047