Tubal ectopic pregnancy occurrence is associated with high expressions of prokineticin receptors and aberrant secretion of inflammatory cytokines

OBJECTIVETubal ectopic pregnancy (TEP) remains the most common cause of maternal morbidity and mortality in the early months of pregnancy. The aim of this study is to perform the correlation between PROKRs and pro-inflammatory genes and explore the role of novel genes in pathogenesis of TEP. METHODS...

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Published in:American journal of translational research Vol. 12; no. 9; pp. 5741 - 5751
Main Authors: Ma, Lin, Li, Zaiyi, Xi, Sujuan, Guo, Quan, Zhao, Panlin, Li, Weihao, Ai, Jing, Chen, Xiaoxuan
Format: Journal Article
Language:English
Published: e-Century Publishing Corporation 01-01-2020
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Summary:OBJECTIVETubal ectopic pregnancy (TEP) remains the most common cause of maternal morbidity and mortality in the early months of pregnancy. The aim of this study is to perform the correlation between PROKRs and pro-inflammatory genes and explore the role of novel genes in pathogenesis of TEP. METHODSHere, quantitative real time PCR and immunohistochemistry were used to assess the expression of the novel genes in 120 TEP patients and 30 age-matched non-TEP patients. The correlation between PROKRs and pro-inflammatory genes were analyzed by Pearson correlation coefficient. Univariate and multivariate Cox regression analyses were used to assess the risk prediction rate of novel genes. Receiver operating characteristic was used to assess the performance of our model. RESULTSPROKRs (PROKR1 and PROKR2) and pro-inflammatory genes (TNF-α, IL-6, and IL-8) expression levels significantly enhanced in TEP patients, and significantly positive correlation with pro-inflammatory genes for PROKRs. A multivariate Cox regression analysis demonstrated that 2 genes (PROKR2 and IL8) had significant diagnostic value, which were associated with the occurrence and development of TEP. CONCLUSIONOur data further denote that dysregulation of PROKR2 and IL-8 were risk factor and played an important role in the pathogenesis of TEP.
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Equal contributors and co-senior authors.
ISSN:1943-8141
1943-8141