Abstract
Inflammation is a biological response of the immune system, which can be triggered by many factors, including pathogens. These factors may induce acute or chronic inflammation in various organs, including the reproductive system, leading to tissue damage or disease. In this study, the RNA-Seq technique was used to determine the in vitro effects of peroxisome proliferator-activated receptor gamma (PPARγ) ligands on the expression of genes and long non-coding RNA, and alternative splicing events (ASEs) in LPS-induced inflammation of the porcine endometrium during the follicular phase of the estrous cycle. Endometrial slices were incubated in the presence of LPS and PPARγ agonists (PGJ2 or pioglitazone) and a PPARγ antagonist (T0070907). We identified 169, 200, 599 and 557 differentially expressed genes after LPS, PGJ2, pioglitazone or T0070907 treatment, respectively. Moreover, changes in differentially expressed long non-coding RNA and differential alternative splicing events were described after the treatments. The study revealed that PPARγ ligands influence the LPS-triggered expression of genes controlling the DNA damage response (GADD45β, CDK1, CCNA1, CCNG1, ATM). Pioglitazone treatment exerted a considerable effect on the expression of genes regulating the DNA damage response.
Highlights
Inflammation is a biological reaction to disrupted tissue homeostasis, caused by interactions between numerous factors[1]
The analysis revealed that nearly 53.64% of the read pairs were mapped to coding sequences, 6.58% were mapped to introns, 24.67% were mapped to untranslated regions, and the remaining 15.11% were mapped to intergenic regions
The present study demonstrated that cyclin A1 (CCNA1) expression in LPS-stimulated porcine endometrium decreased when PPARγ was blocked by the antagonist
Summary
Inflammation is a biological reaction to disrupted tissue homeostasis, caused by interactions between numerous factors[1]. Lipopolysaccharide induces the expression of genes regulating the production of cytokines, adhesion proteins and enzymes involved in pro-inflammatory r esponses[4]. This endotoxin triggers the release of reactive oxygen species (ROS), reactive nitrogen species (RNS) and nitric oxide (NO)[5]. We have demonstrated that PPARγ is involved in LPS-stimulated inflammation of the porcine endometrium during the mid-luteal phase of the estrous c ycle[22]. The aim of the present study was to investigate the in vitro effect of PPARγ ligands (natural or synthetic agonists and an antagonist) on the transcriptome profile of the porcine endometrium during LPS-induced inflammation in the follicular phase of the estrous cycle (days 18–20). The effect of PPARγ ligands on alternative splicing events (ASEs) and long non-coding RNA (lncRNA) expression was analyzed
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