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胚胎热操作通过调节瞬时受体电位 V2 表达增强热应激肉鸡骨骼肌中线粒体功能。

Embryo thermal manipulation enhances mitochondrial function in the skeletal muscle of heat-stressed broilers by regulating transient receptor potential V2 expression.

机构信息

Research Centre for Livestock Environmental Control and Smart Production, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

Research Centre for Livestock Environmental Control and Smart Production, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Poult Sci. 2024 Sep;103(9):104034. doi: 10.1016/j.psj.2024.104034. Epub 2024 Jun 26.

DOI:10.1016/j.psj.2024.104034
PMID:39003798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11298950/
Abstract

Heat stress induces mitochondrial dysfunction, thereby impeding skeletal muscle development and significantly impacting the economic efficiency of poultry production. This study aimed to investigate the effects of embryo thermal manipulation (TM, 41.5°C, 65% RH, 3 h/d during 16-18th embryonic age) on the mitochondrial function of the pectoralis major (PM) in broiler chickens exposed to thermoneutral (24 ± 1°C, 60% RH) or cyclic heat stress (35 ± 1°C, 60% RH, 12 h/d) from day 22 to 28, and to explore potential mechanisms involving transient receptor potential V2 (TRPV2). Additionally, in vitro experiments were conducted to assess the regulatory effects of TRPV2 pharmacological activation and inhibition on mitochondrial function in primary myotubes. The results revealed that TM had no discernible effect on the body weight and feed intake of broiler chickens under heat stress conditions (P > 0.05). However, it did delay the increase in rectal temperature and accelerate the decrease in serum T3 levels (P < 0.05). Furthermore, TM promoted the development of PM muscle fibers, significantly increasing myofiber diameter and cross-sectional area (P < 0.05). Under heat stress conditions, TM significantly upregulated the expression of mitochondrial electron transport chain (ETC) genes and TRPV2 in broiler PM muscle (P < 0.05), with a clear positive correlation observed between the two (P < 0.05). In vitro, pharmacological activation of TRPV2 not only increased its own expression but also enhanced mitochondrial ETC genes expression and oxidative phosphorylation function by upregulating intracellular calcium ion levels (P < 0.05). Conversely, TRPV2 inhibition had the opposite effect. Overall, this study underscores the potential of prenatal thermal manipulation in regulating postnatal broiler skeletal muscle development and mitochondrial function through the modulation of TRPV2 expression.

摘要

热应激会导致线粒体功能障碍,从而阻碍骨骼肌的发育,并显著影响家禽生产的经济效益。本研究旨在探讨胚胎热处理(TM,41.5°C,65%RH,16-18 日龄每天 3 小时)对在 22-28 日龄时处于热中性(24±1°C,60%RH)或周期性热应激(35±1°C,60%RH,12 小时/天)条件下的肉鸡胸肌(PM)线粒体功能的影响,并探讨涉及瞬时受体电位 V2(TRPV2)的潜在机制。此外,还进行了体外实验,以评估 TRPV2 药理学激活和抑制对原代肌管中线粒体功能的调节作用。结果表明,TM 对热应激条件下肉鸡的体重和采食量没有明显影响(P>0.05)。然而,它确实延迟了直肠温度的升高并加速了血清 T3 水平的下降(P<0.05)。此外,TM 促进了 PM 肌肉纤维的发育,显著增加了肌纤维直径和横截面积(P<0.05)。在热应激条件下,TM 显著上调了肉鸡 PM 肌肉中线粒体电子传递链(ETC)基因和 TRPV2 的表达(P<0.05),两者之间存在明显的正相关(P<0.05)。在体外,TRPV2 的药理学激活不仅增加了自身的表达,还通过增加细胞内钙离子水平增强了线粒体 ETC 基因的表达和氧化磷酸化功能(P<0.05)。相反,TRPV2 抑制则产生相反的效果。总的来说,本研究强调了产前热处理通过调节 TRPV2 表达在调节产后肉鸡骨骼肌发育和线粒体功能方面的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/c1c2cc352249/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/2f0116729775/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/560142bb4622/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/194a3244f35a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/1cdb0761427c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/b748a54abb67/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/70b6107ffe84/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/b72b90aec22b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/c1c2cc352249/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/2f0116729775/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/560142bb4622/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/194a3244f35a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/1cdb0761427c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/b748a54abb67/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/70b6107ffe84/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/b72b90aec22b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1649/11298950/c1c2cc352249/gr8.jpg

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