Surfactant protein-C (SP-C) increases the surface adsorption and lowers surface tension of lung surfactant. SP-C binds lipopolysaccharide (LPS) and interacts with CD-14, required for TLR4 signaling. SP-C polymorphism associates with susceptibility to RDS and possibly to preterm birth.1 However, SP-C expression may not be restricted to lung. Here we investigate further the involvement of SP-C during perinatal adaptation.
Systemic inflammatory response and spontaneous preterm birth were induced in timed-pregnant C57BL/6 mice by intraperitoneal LPS on day 17 of gestation to induce systemic inflammatory response and spontaneous preterm birth (SPB).2 RNase protection assay and RT-PCR were used to quantitatively determine SP-C mRNA and protein was detected by the Western blot. The SP-C Thr138Asn polymorphism was studied in 304 mothers with spontaneous preterm birth and in 386 of their preterm children. 202 mothers and 199 children with exclusively term births served as controls.
SP-C mRNA was detected in mouse uterus, placenta and fetal membranes and in human placenta, amnion and chorion. An increase in the expression of SP-C was detected in placenta, uterus and fetal membranes after LPS challenge. SP-C polymorphism did not associate with SPB. However, in families with multiple SPB and abortion, the minor allele was prevalent.
SP-C mRNA and proSP-C were detected in mouse uterus, placenta and fetal membranes and LPS increased the expression. We propose that, besides the neonatal respiratory adaption, SP-C may be involved in the perinatal transition.
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