Guo Xinyi, Ying Shijia, Xiao Huiping, An Hao, Guo Rihong, Dai Zichun, Wu Wenda
MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China.
Metabolites. 2024 Jun 27;14(7):362. doi: 10.3390/metabo14070362.
Lipopolysaccharide (LPS) is one of the important pathogenic substances of and , which causes injury to the reproductive system. Ovarian dysfunction due to Gram-negative bacterial infections is a major cause of reduced reproductive performance in geese. However, the specific molecular mechanisms of LPS-induced impairment of sex steroid hormone synthesis have not been determined. The regulatory mechanism of miRNA has been proposed in many physiological and pathogenic mechanisms. Therefore, the role of miRNA in breeding geese exposed to LPS during the peak laying period was investigated. In this study, twenty Yangzhou geese at peak laying period were injected with LPS for 0 h, 24 h, and 36 h. The follicular granulosa layer was taken for RNA-seq and analyzed for differentially expressed miRNAs. It was observed that LPS changed the appearance of hierarchical follicles. miRNA sequencing analysis was applied, and miR-21 and SMAD2 (SMAD family member 2) were selected from 51 differentially expressed miRNAs through bioinformatics prediction. The results showed that miR-21 down-regulated SMAD2 expression and progesterone (P4) production in LPS-treated goose granulosa cells (GCs). It also determined that overexpression of miR-21 or silence of SMAD2 suppressed the sex steroid biosynthesis pathway by decreasing STAR and CYP11A1 expression. Down-regulation of miR-21 exacerbates the LPS-induced decline in P4 synthesis and vice versa. The findings indicated that miR-21 was involved in LPS regulation of P4 synthesis in goose granulosa cells by down-regulating SMAD2. This study provides theoretical support for the prevention of LPS-induced ovarian dysfunction in geese.
脂多糖(LPS)是[具体细菌名称1]和[具体细菌名称2]的重要致病物质之一,可导致生殖系统损伤。革兰氏阴性菌感染引起的卵巢功能障碍是鹅繁殖性能下降的主要原因。然而,LPS诱导性类固醇激素合成受损的具体分子机制尚未确定。miRNA的调控机制已在许多生理和致病机制中被提出。因此,研究了miRNA在产蛋高峰期暴露于LPS的种鹅中的作用。在本研究中,对20只处于产蛋高峰期的扬州鹅分别注射LPS 0小时、24小时和36小时。采集卵泡颗粒层进行RNA测序,并分析差异表达的miRNA。观察到LPS改变了等级卵泡的外观。应用miRNA测序分析,并通过生物信息学预测从51个差异表达的miRNA中筛选出miR-21和SMAD2(SMAD家族成员2)。结果表明,miR-21下调LPS处理的鹅颗粒细胞(GCs)中SMAD2的表达和孕酮(P4)的产生。还确定miR-21的过表达或SMAD2的沉默通过降低STAR和CYP11A1的表达抑制性类固醇生物合成途径。miR-21的下调加剧了LPS诱导的P4合成下降,反之亦然。研究结果表明,miR-21通过下调SMAD2参与LPS对鹅颗粒细胞中P4合成的调控。本研究为预防LPS诱导的鹅卵巢功能障碍提供了理论支持。