Differential proteomics of placentas reveals metabolic disturbance and oxidative damage participate yak spontaneous miscarriage during late pregnancy

Background High spontaneous miscarriage rate in yak, especially during late pregnancy, have caused a great economic loss to herdsmen living in the Qinghai-Tibet plateau. However, the mechanism underlying spontaneous miscarriage is still poorly understood. In the present study, placenta protein markers were identified to elucidate the pathological reasons for yak spontaneous miscarriage through isobaric tags for relative and absolute quantification (iTRAQ) proteomic technology and bioinformatic approaches. Results Subsequently, a total of 415 differentially expressed proteins (DEPs) were identified between aborted and normal placentas. The up-regulated DEPs in the aborted placentas were significantly associated with spinocerebellar ataxia, sphingolipid signalling, relaxin signalling, protein export, protein digestion and absorption and aldosterone synthesis and secretion pathway. While the down-regulated DEPs in the aborted placentas mainly participated in valine, leucine and isoleucine degradation, PPAR signalling, peroxisome, oxidative phosphorylation, galactose metabolism, fatty acid degradation, cysteine and methionine metabolism and citrate cycle pathway. Conclusions The results implied that the identified DEPs could be considered as placental protein markers for yak miscarriage during late pregnancy, and biomacromolecule metabolic abnormality and oxidative damage might be responsible for the high spontaneous miscarriage rate in yak. These findings provide an important theoretical basis for deciphering the pathologic mechanism of late spontaneous miscarriage in yak.

Automated summary

In this study, placental protein markers for yak spontaneous miscarriage were identified using proteomic technology and bioinformatics. Abnormalities in biomacromolecule metabolism and oxidative damage were found to be responsible for the high spontaneous miscarriage rate in yak.