Faculty of Animal Science and Technology, Gansu Agricultural University, Lanzhou, 730070, People's Republic of China.
Biol Trace Elem Res. 2024 Mar;202(3):1187-1202. doi: 10.1007/s12011-023-03731-y. Epub 2023 Jun 27.
Heat stress threatens severely cardiac function by caused myocardial injury in poultry. Our previous study has showed that manganese (Mn) has a beneficial effect on heat-stress resistance of broiler. Therefore, we tried to confirm the alleviation mechanism through proteomic analysis after heat stress exposure to primary broiler myocardial cells pretreated with Mn. The experiment was divided into four groups: CON group (37 °C, cells without any treatment), HS group (43 °C, cells treatment with heat stress for 4 h), HS+MnCl group (cells treated with 20 μM MnCl before heat stress), and HS+Mn-AA group (cells treated with 20 μM Mn compound amino acid complex before heat stress). Proteome analysis using DIA identified 300 differentially expressed proteins (DEPs) between CON group and HS group; 93 and 121 DEPs were identified in inorganic manganese treatment group and organic manganese treatment group, respectively; in addition, there were 53 DEPs identified between inorganic and organic manganese group. Gene Ontology (GO) analysis showed that DEPs were mainly involved in binding, catalytic activity, response to stimulus, and metabolic process. DEPs of manganese pretreatment involved in a variety of biological regulatory pathways, and significantly influenced protein processing and repair in endoplasmic reticulum, apoptosis, and DNA replication and repair. These all seem to imply that manganese may help to resist cell damage induced by heat stress by regulating key node proteins. These findings contribute to a better understanding of the effects of manganese on overall protein changes during heat-stress and the possible mechanisms, as well as how to better use manganese to protect heart function in high temperature.
热应激通过引起家禽心肌损伤严重威胁心脏功能。我们之前的研究表明,锰(Mn)对肉鸡的耐热性有有益影响。因此,我们试图通过对用 Mn 预处理的原代肉鸡心肌细胞进行热应激暴露后的蛋白质组学分析来确认缓解机制。该实验分为四组:CON 组(37°C,未经任何处理的细胞)、HS 组(43°C,用热应激处理 4 小时的细胞)、HS+MnCl 组(用 20μM MnCl 处理细胞之前热应激)和 HS+Mn-AA 组(用 20μM Mn 复合氨基酸复合物处理细胞之前热应激)。使用 DIA 的蛋白质组分析鉴定出 CON 组和 HS 组之间的 300 个差异表达蛋白(DEPs);在无机锰处理组和有机锰处理组中分别鉴定出 93 和 121 个 DEPs;此外,在无机和有机锰组之间鉴定出 53 个 DEPs。基因本体论(GO)分析表明,DEPs 主要参与结合、催化活性、对刺激的反应和代谢过程。锰预处理的 DEPs 涉及多种生物调节途径,并显著影响内质网中的蛋白质加工和修复、细胞凋亡以及 DNA 复制和修复。所有这些似乎都暗示,锰可能通过调节关键节点蛋白来帮助抵抗热应激引起的细胞损伤。这些发现有助于更好地理解锰在热应激过程中对整体蛋白质变化的影响及其可能的机制,以及如何更好地利用锰来保护高温下的心脏功能。