To study the relationship between pulmonary surfactant-associated protein B (SP-B) gene polymorphisms and their susceptibility to neonatal respiratory distress syndrome (RDS).
Eighty-eight preterm infants with RDS (RDS group) and 103 infants without RDS (control group) were enrolled. The genomic DNA was isolated using DNA kits. Polymerase chain reaction with restriction fragment length polymorphism technique was used to detect the genotype and allele frequency of the SP-B -18A/C and SP-B 1580C/T single nucleotide polymorphisms. The association between the polymorphisms and RDS was analyzed.
SP-B -18A/C and SP-B 1580C/T were found to be polymorphic in both RDS and control groups. The frequencies of CC genotype (X2=12.26, P<0.01) and C allele (X2=11.97, P<0.01) of SP-B 1580C/T were significantly higher in the RDS group than in the control group. The C allele significantly increased the risk of RDS (OR=2.26, 95%CI: 1.42-3.60). The frequencies of genotype and allele of SP-B -18A/C showed no significant difference between the two groups.
SP-B 1580C/T polymorphism contributes to the etiology of RDS and may serve as the susceptibility gene for RDS. The C allele increases the risk of RDS. SP-B -18A/C shows no association with the etiology of RDS.
"SP-B is an important pulmonary surfactant-associated protein capable of reducing or altering the surface tension by changing the surface area, preventing alveolar collapse (1–3). Studies have shown SP-B protein deficiency to be associated with the pathogenesis of neonatal respiratory distress syndrome (RDS) (4,5). The protein expression is known to be regulated by upstream genes. "
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to investigate whether surfactant-associated protein B (SP-B) mRNA deficiency is involved in the pathogenesis of neonatal respiratory distress syndrome (RDS). A total of 60 unrelated neonates who died of RDS were recruited as the RDS group and subgrouped into a ≤32-, a 32-36(+6)- and a ≥37-week group (n=20 per group) on the basis of gestational age. In addition, 60 neonates who succumbed to other diseases were enrolled as controls. The lung tissues were collected within 30 min after death. In situ hybridization was conducted to detect SP-B mRNA expression in the lung. The frequency of SP-B mRNA deficiency was also calculated. Among the RDS groups, the SP-B mRNA levels were significantly higher compared to those in the control group (t=7.812, P<0.001), but were comparable among RDS patients with different gestational ages (F=2.348, P>0.105). Among the control groups, the SP-B mRNA levels increased with the increase in gestational age (F=50.124, P<0.001). In the ≤32-week group, the number of cells positive for SP-B mRNA in RDS patients was markedly reduced as compared to that of the controls (t=3.185, P<0.01). In the 32-36(+6)-week group, the number of cells positive for SP-B mRNA in RDS patients was significantly smaller compared to that of the controls (t=9.342, P<0.001). In the ≥37-week group, the number of cells positive for SP-B mRNA in RDS patients was markedly smaller compared to that in the controls (t=4.238, P<0.001). Among RDS neonates, SP-B mRNA deficiency was noted in 35 patients with a frequency of 58.3%. In the control group, SP-B mRNA deficiency was noted in 8 patients with a frequency of 13.3%, which was markedly lower compared to that in the RDS group (χ(2)=26.421, P<0.001). The results of the present study therefore suggest that SP-B mRNA deficiency is involved in the pathogenesis of RDS.
Experimental and therapeutic medicine 11/2012; 4(5):815-819. DOI:10.3892/etm.2012.673 · 1.27 Impact Factor
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