Liu Runfeng, Huang Xingchen, Sun Qinqiang, Hou Zhen, Yang Weihan, Zhang Junjun, Zhang Pengfei, Huang Liangfeng, Lu Yangqing, Fu Qiang
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530004, China.
Animals (Basel). 2022 Jul 1;12(13):1706. doi: 10.3390/ani12131706.
The acquisition of mammalian sperm motility is a main indicator of epididymal sperm maturation and helps ensure fertilization. Poor sperm motility will prevent sperm cells from reaching the fertilization site, resulting in fertilization failure. To investigate the proteomic profiling of normal and poorly motile buffalo spermatozoa, a strategy applying liquid chromatography tandem mass spectrometry combined with tandem mass targeting was used. As a result, 145 differentially expressed proteins (DEPs) were identified in poorly motile spermatozoa (fold change > 1.5), including 52 upregulated and 93 downregulated proteins. The upregulated DEPs were mainly involved in morphogenesis and regulation of cell differentiation. The downregulated DEPs were involved with transport, oxidation-reduction, sperm motility, regulation of cAMP metabolism and regulation of DNA methylation. The mRNA and protein levels of PRM1 and AKAP3 were lower in poorly motile spermatozoa, while the expressions of SDC2, TEKT3 and IDH1 were not correlated with motility, indicating that their protein changes were affected by transcription or translation. Such changes in the expression of these proteins suggest that the formation of poorly motile buffalo spermatozoa reflects a low efficiency of energy metabolism, decreases in sperm protamine proteins, deficiencies in motility-related proteins, and variations in tail structural proteins. Such proteins could be biomarkers of poorly motile spermatozoa. These results illustrate some of the molecular mechanisms associated with poorly motile spermatozoa and provide clues for finding molecular markers of these pathways.
哺乳动物精子活力的获得是附睾精子成熟的主要指标，有助于确保受精。精子活力差会阻止精子细胞到达受精部位，导致受精失败。为了研究正常和活力差的水牛精子的蛋白质组图谱，采用了液相色谱串联质谱结合串联质谱靶向的策略。结果，在活力差的精子中鉴定出145种差异表达蛋白（DEP）（倍数变化>1.5），其中52种上调，93种下调。上调的DEP主要参与形态发生和细胞分化的调控。下调的DEP与转运、氧化还原、精子活力、cAMP代谢调控和DNA甲基化调控有关。活力差的精子中PRM1和AKAP3的mRNA和蛋白水平较低，而SDC2、TEKT3和IDH1的表达与活力无关，表明它们的蛋白质变化受转录或翻译影响。这些蛋白质表达的变化表明，活力差的水牛精子的形成反映了能量代谢效率低下、精子鱼精蛋白减少、活力相关蛋白缺乏以及尾部结构蛋白的变化。这些蛋白质可能是活力差的精子的生物标志物。这些结果阐明了一些与活力差的精子相关的分子机制，并为寻找这些途径的分子标记提供了线索。
