在青藏高原,生长迟缓的牦牛所占比例很高,减少了农民的经济收入。我们以前的研究发现了生长迟缓的牦牛的瘤胃上皮发育异常,但分子机制尚不清楚。这项研究旨在揭示瘤胃上皮中的蛋白质组学特征如何导致牦牛的生长迟缓。使用高分辨率质谱仪检测瘤胃上皮的蛋白质组。生长迟缓的牦牛和生长正常的牦牛的瘤胃上皮中有52种蛋白质表达显着差异,生长迟缓的牦牛中有32头下调,20头上调。功能分析显示不同表达的蛋白质参与酮体的合成和降解(p=0.012),丙酸代谢(p=0.018),丙酮酸代谢(p=0.020),和矿物质吸收(p=0.024)。SLC26A3和FTH1蛋白的表达,富集了矿物质的吸收,在生长迟缓的牦牛中显著下调。酮体合成中富集的关键酶ACAT2和HMGCS2和丙酸代谢中富集的关键酶PCCA在生长迟缓的牦牛瘤胃上皮中蛋白表达较低。生长正常牦牛瘤胃上皮的ATP浓度和相对线粒体DNA拷贝数显著高于生长迟缓牦牛(p<0.05)。柠檬酸合酶(CS)的活性,α-酮戊二酸脱氢酶复合物(α-KGDHC),三羧酸循环(TCA)中的异柠檬酸脱氢酶(ICD),与生长正常的牦牛相比,生长迟缓的牦牛的瘤胃上皮中线粒体呼吸链复合物(MRCC)显着降低(p<0.05)。COQ9、COX4和LDHA的mRNA表达,它们是MRCC中的编码基因,IV和无氧呼吸,在生长迟缓的牦牛的瘤胃上皮中也显着降低(p<0.05)。相关分析表明,平均日增重(ADG)与瘤胃上皮中相对线粒体DNA拷贝数(p<0.01,r=0.772)和ATP浓度(p<0.01,r=0.728)呈显着正相关。分别。瘤胃重量与相对线粒体DNA拷贝数(p<0.05,r=0.631)和瘤胃上皮ATP浓度(p<0.01,r=0.957)呈正相关,分别。瘤胃乳头与瘤胃上皮ATP浓度呈显著正相关(p<0.01,r=0.770)。这些结果表明,生长迟缓的牦牛具有较低的VFA代谢,酮体合成,离子吸收,瘤胃上皮细胞ATP合成与瘤胃上皮细胞ATP合成受阻有关。
Growth-retarded
yaks are of a high proportion on the Tibetan plateau and reduce the economic income of farmers. Our previous studies discovered a maldevelopment in the ruminal epithelium of growth-retarded
yaks, but the molecular mechanisms are still unclear. This study aimed to reveal how the proteomic profile in the ruminal epithelium contributed to the growth retardation of yaks. The proteome of the ruminal epithelium was detected using a high-resolution mass spectrometer. There were 52 proteins significantly differently expressed between the ruminal epithelium of growth-retarded yaks and growth-normal
yaks, with 32 downregulated and 20 upregulated in growth-retarded
yaks. Functional analysis showed the differently expressed proteins involved in the synthesis and degradation of ketone bodies (p = 0.012), propanoate metabolism (p = 0.018), pyruvate metabolism (p = 0.020), and mineral absorption (p = 0.024). The protein expressions of SLC26A3 and FTH1, enriched in the mineral absorption, were significantly downregulated in growth-retarded yaks. The key enzymes ACAT2 and HMGCS2 enriched in ketone bodies synthesis and key enzyme PCCA enriched in propanoate metabolism had lower protein expressions in the ruminal epithelium of growth-retarded yaks. The ATP concentration and relative mitochondrial DNA copy number in the ruminal epithelium of growth-normal yaks were dramatically higher than those of growth-retarded
yaks (p < 0.05). The activities of citrate synthase (CS), the α-ketoglutarate dehydrogenase complex (α-KGDHC), isocitrate dehydrogenase (ICD) in the tricarboxylic acid cycle (TCA), and the mitochondrial respiratory chain complex (MRCC) were significantly decreased in ruminal epithelium of growth-retarded yaks compared to growth-normal
yaks (p < 0.05). The mRNA expressions of COQ9, COX4, and LDHA, which are the encoding genes in MRCC I, IV and anaerobic respiration, were also significantly decreased in the ruminal epithelium of growth-retarded yaks (p < 0.05). Correlation analysis revealed that the average daily gain (ADG) was significantly positively correlated to the relative mitochondrial DNA copy number (p < 0.01, r = 0.772) and ATP concentration (p < 0.01, r = 0.728) in the ruminal epithelium, respectively. The ruminal weight was positively correlated to the relative mitochondrial DNA copy number (p < 0.05, r = 0.631) and ATP concentration in ruminal epithelium (p < 0.01, r = 0.957), respectively. The ruminal papillae had a significant positive correlation with ATP concentration in ruminal epithelium (p < 0.01, r = 0.770). These results suggested that growth-retarded yaks had a lower VFA metabolism, ketone bodies synthesis, ion absorption, and ATP synthesis in the ruminal epithelium; it also indicated that the growth retardation of yaks is related to the obstruction of cellular ATP synthesis in rumen epithelial cells.