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  • Developmental and genetic regulation of human surfactant protein B in vivo. 18776725

    Genetic and developmental disruption of surfactant protein B (SP-B) expression causes neonatal respiratory distress syndrome (RDS).To assess developmental and genetic regulation of SP-B expression in vivo.To evaluate in vivo developmental regulation of SP-B, we used immunoblotting to compare frequency of detection of mature and pro-SP-B peptides in developmentally distinct cohorts: 24 amniotic fluid samples, unfractionated tracheal aspirates from 101 infants greater than or=34 weeks' gestation with (75) and without (26) neonatal RDS, and 6 nonsmoking adults. To examine genetic regulation, we used univariate and logistic regression analyses to detect associations between common SP-B (SFTPB) genotypes and SP-B peptides in the neonatal RDS cohort.We found pro-SP-B peptides in 24/24 amniotic fluid samples and in 100/101 tracheal aspirates from newborn infants but none in bronchoalveolar lavage from normal adults (0/6) (p less than 0.001). We detected an association (p = 0.0011) between pro-SP-B peptides (M(r) 40 and 42 kDa) and genotype of a nonsynonymous single nucleotide polymorphism at genomic position 1580 that regulates amino-terminus glycosylation.Pro-SP-B peptides are more common in developmentally less mature humans. Association of genotype at genomic position 1580 with pro-SP-B peptides (M(r) 40 and 42 kDa) suggests genetic regulation of amino terminus glycosylation in vivo.
    Document Type:
    Reference
    Product Catalog Number:
    AB3430
    Product Catalog Name:
    Anti-Prosurfactant Protein B Antibody, reacts with both CT and NT

  • Ezrin distribution is abnormal in principal cells from a murine model of autosomal recessive polycystic kidney disease. 12840161

    Abnormalities in cell proliferation and intracellular signaling are features of inherited human and murine polycystic kidney diseases (PKD), regardless of the primary genetic defects. Loss of protein kinase A regulation of cell proliferation has been reported in the murine C57BL/6JCys1cpk-/- (cpk) model of autosomal recessive PKD. Qualitative differences in protein kinase A subunit distribution were observed between filter-grown cultures of noncystic- (C57BL/6J mice) and cystic cpk-derived principal cells. It was hypothesized that protein kinase A subunit distribution differences were mediated by differences in A-kinase anchoring protein (AKAP) expression, so expression of four AKAPs was examined in filter-grown cultures of primary murine cystic- and noncystic-derived principal cells. AKAP-KL expression was ambiguous, but mAKAP, AKAP95, and ezrin were expressed at expected molecular sizes and cellular locations in noncystic-derived cells. Perinuclear mAKAP and nuclear AKAP95 were distributed normally in cpk-derived cells. Expression of AKAP95 in cystic epithelium was diminished relative to controls, and ezrin expression was modestly decreased and abnormally distributed within a region near the apical surface. Qualitative differences were observed in ezrin location in response to medium change or stimulation with epidermal growth factor which suggested cell-specific differences may result from the cpk mutation or the abnormal epidermal growth factor receptor phenotype that characterizes PKD. Ezrin has been implicated in tubulogenesis, so altered ezrin expression or function could be disruptive. If PKD mutations that contribute to PKD pathogenesis are postulated to disrupt normal tubular development, perhaps the mechanism includes altered ezrin function and abnormal protein kinase A targeting.
    Document Type:
    Reference
    Product Catalog Number:
    07-087