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Updated: May 28, 2025
A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
Elevated expression and reduced phosphorylation of uterine RIG-I protein in a murine model of pathogenic preterm
Unlike TLRs, the regulation of RLRs in PTL is not well understood. It is unclear if the RLR pathway is activated in uterine tissue during PTL and whether this activation is specific to pathogenic agents. This study aimed to elucidate the regulation of the RLR pathway in two PTL models. On gestation day 16, PTL was induced in mice using lipopolysaccharide (LPS) for pathogenic inflammation and RU486, a progesterone antagonist, for nonpathogenic inflammation. PTL and fetal viability rates were assessed, and uterine tissue was collected for ELISA, real-time PCR, immunohistochemistry for RIG-I, and Western blot analysis of RIG-I and downstream proteins. Spontaneous and agonist-induced uterine contractility were also evaluated. PTL was induced 8-10 h after LPS and 16-18 h after RU486 administration. Histopathological analysis showed inflammatory changes and neutrophilic infiltration in uterine tissues. Peripheral leukocyte count, TNFα, and IL-6 levels were significantly higher in both LPS- and RU486-treated groups. Agonist-induced uterine contractility was notably reduced in LPS-treated mice. RIG-I mRNA and protein expressions were significantly elevated in LPS-treated animals, with decreased RIG-I phosphorylation, while RU486 treatment did not affect these parameters. IRF3 expression and its phosphorylation demonstrated significant upregulation in both PTL models. In addition, interferon-β and lactate levels were elevated in both groups. The findings suggest that the RLR pathway is activated specifically in the pathogenic model of murine PTL through increased RIG-I expression and decreased phosphorylation.
In Brief:
Preterm labor (PTL) is strongly associated with maternal inflammation, an innate immune response. This study demonstrates that the RIG-I-like receptor (RLR) pathway, a key element of innate immunity, is specifically activated in cases of pathogenic PTL.
Unlike TLRs, the regulation of RLRs in PTL is not well understood. It is unclear if the RLR pathway is activated in uterine tissue during PTL and whether this activation is specific to pathogenic agents. This study aimed to elucidate the regulation of the RLR pathway in two PTL models. On gestation day 16, PTL was induced in mice using lipopolysaccharide (LPS) for pathogenic inflammation and RU486, a progesterone antagonist, for nonpathogenic inflammation. PTL and fetal viability rates were assessed, and uterine tissue was collected for ELISA, real-time PCR, immunohistochemistry for RIG-I, and Western blot analysis of RIG-I and downstream proteins. Spontaneous and agonist-induced uterine contractility were also evaluated. PTL was induced 8-10 h after LPS and 16-18 h after RU486 administration. Histopathological analysis showed inflammatory changes and neutrophilic infiltration in uterine tissues. Peripheral leukocyte count, TNFα, and IL-6 levels were significantly higher in both LPS- and RU486-treated groups. Agonist-induced uterine contractility was notably reduced in LPS-treated mice. RIG-I mRNA and protein expressions were significantly elevated in LPS-treated animals, with decreased RIG-I phosphorylation, while RU486 treatment did not affect these parameters. IRF3 expression and its phosphorylation demonstrated significant upregulation in both PTL models. In addition, interferon-β and lactate levels were elevated in both groups. The findings suggest that the RLR pathway is activated specifically in the pathogenic model of murine PTL through increased RIG-I expression and decreased phosphorylation.
