Disruption of the SP-A/SP-R210 < sub > L < /sub > (Myo18A α) pathway prolongs gestation and reduces fetal survival during lipopolysaccharide-induced parturition in late gestation

We report that either lack of SP-A or disruption of SP-R210L delays parturition by 0.40 and 0.55 days compared to controls, respectively. LPS induced labor 0.60, 1.01, 0.40, 1.00, and 1.31 days earlier than PBS controls in WT, SP-A-deficient, littermate controls, heterozygous, and homozygous SP-R210L-deficient mice, respectively. Lack of SP-A reduced litter size in PBS-treated mice, whereas the total number of pups delivered was similar in all LPS-treated mice. The number of live pups, however, was significantly reduced by 50-70% in SP-A and SP-R210L-deficient mice compared to controls. Differences in gestational length were not associated with intrauterine growth restriction. The present findings support the novel concept that the SP-A/SP-R210 pathway modulates timely labor and delivery and supports fetal lung barrier integrity during fetal to neonatal transition in term pregnancy.PMID:38349123 | DOI:10.1152/ajplung.00383.2023
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - Category: Cytology Authors: Source Type: research