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转录组分析揭示了肉鸡自发性胫骨软骨发育不良的发病机制。

Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers.

作者信息

Shi Kai, Wu Yongfu, Jiang Xusheng, Liu Xiangping, Du Yuesong, Feng Chungang, Li Dongfeng

机构信息

College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, Jiangsu, China.

Ningbo Academy of Agricultural Sciences, Ningbo, China.

出版信息

Front Genet. 2024 Jul 29;15:1434532. doi: 10.3389/fgene.2024.1434532. eCollection 2024.

DOI:10.3389/fgene.2024.1434532
PMID:39139824
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11320418/
Abstract

Tibial dyschondroplasia (TD) is a severe bone disease that affects fast-growing broiler chickens and causes economic loss. Despite previous studies, the regulatory mechanism of TD remains unclear and is thought to be primarily based on thiram induction, which may differ from that of naturally occurring diseases. To better understand TD, a digital X-ray machine was used in the present study to determine its incidence in four hundred yellow-feathered broiler chickens. The results showed that the incidence of TD was 22% after 6 weeks and gradually decreased after 8 and 10 weeks. The body weight of broilers with TD decreased significantly compared to that of NTD broilers. In addition, the length and density of the tibia were reduced after eight and 10 weeks, and the density of the tibia was reduced after 6 weeks compared with the NTD chickens. This study also examined tibial quality parameters from TD (n = 12) and NTD broilers (n = 12) and found that bone mineral content, bone mineral density, bone ash content, calcium content, and phosphorus content were significantly reduced in TD broilers. Transcriptome analysis revealed 849 differentially expressed genes (DEGs) in the growth plate between TD (n = 6) and NTD groups (n = 6). These genes were enriched in ECM-receptor interaction, cytokine-cytokine receptor interaction, calcium signaling pathway, and TGF-β signaling. Genes encoding the alpha chain of type XII collagen, that is, , , and ) were identified as critical in the regulatory network of TD. Gene set enrichment analysis (GSEA) revealed that the pathways of cartilage development, circulatory system development, and nervous system development were changed in the growth plates of TD birds. In the blood transcriptome, 12 DEGs were found in TD (n = 4) and NTD chickens (n = 4), and GSEA revealed that the pathways from TD broilers' blood related to the phagosome, linoleic acid metabolism, monoatomic ion homeostasis, and calcium ion transport were downregulated. This study provides a comprehensive understanding of TD, including its effects on tibial quality, tibial changes, and the circulatory system, along with identifying important genes that may lead to the development of TD.

摘要

胫骨软骨发育不良(TD)是一种严重的骨骼疾病,会影响快速生长的肉鸡并造成经济损失。尽管此前已有研究,但TD的调控机制仍不明确,且被认为主要基于福美双诱导,这可能与自然发生的疾病不同。为了更好地了解TD,本研究使用数字X光机来确定其在400只黄羽肉鸡中的发病率。结果显示,6周后TD的发病率为22%,8周和10周后逐渐下降。与无TD的肉鸡相比,患TD的肉鸡体重显著下降。此外,8周和10周后胫骨的长度和密度降低,6周后与无TD的鸡相比胫骨密度降低。本研究还检测了TD组(n = 12)和无TD肉鸡组(n = 12)的胫骨质量参数,发现TD肉鸡的骨矿物质含量、骨矿物质密度、骨灰含量、钙含量和磷含量均显著降低。转录组分析揭示了TD组(n = 6)和无TD组(n = 6)生长板中849个差异表达基因(DEG)。这些基因富集于细胞外基质-受体相互作用、细胞因子-细胞因子受体相互作用、钙信号通路和TGF-β信号通路。编码 XII 型胶原α链的基因,即 、 和 ,被确定为TD调控网络中的关键基因。基因集富集分析(GSEA)显示,TD鸡生长板中软骨发育、循环系统发育和神经系统发育的通路发生了变化。在血液转录组中,TD组(n = 4)和无TD鸡组(n = 4)中发现了12个DEG,GSEA显示TD肉鸡血液中与吞噬体、亚油酸代谢、单原子离子稳态和钙离子转运相关的通路被下调。本研究全面了解了TD,包括其对胫骨质量、胫骨变化和循环系统的影响,同时确定了可能导致TD发生的重要基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/9765840d5fe5/fgene-15-1434532-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/6ee79379b4cf/fgene-15-1434532-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/0f5c53cec4c6/fgene-15-1434532-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/9765840d5fe5/fgene-15-1434532-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/6ee79379b4cf/fgene-15-1434532-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/0f5c53cec4c6/fgene-15-1434532-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c378/11320418/9765840d5fe5/fgene-15-1434532-g003.jpg

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本文引用的文献

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Pestic Biochem Physiol. 2024 May;201:105847. doi: 10.1016/j.pestbp.2024.105847. Epub 2024 Mar 15.
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The autophagy-mediated mechanism via TSC1/mTOR signaling pathway in thiram-induced tibial dyschondroplasia of broilers.他莫昔芬诱导的肉鸡胫骨软骨发育不良中 TSC1/mTOR 信号通路介导的自噬机制。
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Molecular mechanism of miR-203a targeting Runx2 to regulate thiram induced-chondrocyte development.
miR-203a 靶向 Runx2 调控代森锰锌诱导的软骨细胞发育的分子机制。
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miR-206a-3p suppresses the proliferation and differentiation of chicken chondrocytes in tibial dyschondroplasia by targeting BMP6.miR-206a-3p 通过靶向 BMP6 抑制胫骨软骨发育不良鸡软骨细胞的增殖和分化。
Poult Sci. 2024 Apr;103(4):103534. doi: 10.1016/j.psj.2024.103534. Epub 2024 Feb 7.
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Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia.胫骨软骨发育不良中通过刺猬信号通路、Notch网格和 Ephrin 信号通路对促血管生成和抗血管生成蛋白的稳态调节
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miR-181b-1-3p affects the proliferation and differentiation of chondrocytes in TD broilers through the WIF1/Wnt/β-catenin pathway.微小RNA-181b-1-3p通过WIF1/ Wnt/β-连环蛋白信号通路影响TD肉鸡软骨细胞的增殖和分化。
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