Hormonal Regulation of Surfactant Protein-B and Surfactant Protein-C Gene Expression in Fetal Lung

2003 ◽  
pp. 81-90 ◽  
Author(s):  
Vijayakumar Boggaram
Keyword(s):  
Gene Expression ◽  
Hormonal Regulation ◽  
Protein C ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Surfactant Protein C ◽  
Surfactant Protein B ◽  
Protein B

Effect of Dexamethasone on Gene Expression of Surfactant Protein B and Surfactant Protein C

2003 ◽  
Vol 54 (4) ◽  
pp. 439
Author(s):  
Ik Soo Park ◽  
Jang Won Sohn ◽  
Ho Joo Yoon ◽  
Dong Ho Shin ◽  
Sung Soo Park
Keyword(s):  
Gene Expression ◽  
Protein C ◽  
Surfactant Protein ◽  
Surfactant Protein C ◽  
Surfactant Protein B ◽  
Protein B

Rabbit surfactant protein C: cDNA cloning and regulation of alternatively spliced surfactant protein C mRNAs

1992 ◽  
Vol 263 (6) ◽  
pp. L634-L644 ◽  
Author(s):  
V. Boggaram ◽  
R. K. Margana
Keyword(s):  
Gene Expression ◽  
Lung Development ◽  
Genomic Dna ◽  
Protein C ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Surfactant Protein C ◽  
Fetal Lung Development ◽  
Mrna Content

Surfactant protein C (SP-C), a hydrophobic protein of pulmonary surfactant is essential for surfactant function. Toward elucidating molecular mechanisms that mediate regulation of SP-C gene expression in rabbit lung, we isolated and characterized cDNAs encoding rabbit SP-C and studied the regulation of SP-C gene expression during fetal lung development and by adenosine 3',5'-cyclic monophosphate (cAMP) and dexamethasone in fetal lung tissues in vitro. We found that rabbit SP-C is highly homologous to SP-C of other species and is encoded by two mRNAs that differ by an insertion of 31 nucleotides in the 3' untranslated regions. SP-C mRNAs were classified into two types based on the nucleotide sequence; type I represents RNA without the 31 nucleotide insert and comprises approximately 80–90% of total SP-C mRNA content, whereas type II represents RNA containing the insert and comprises approximately 10–20% of total SP-C mRNA content. SP-C mRNAs were induced in a coordinate manner during fetal lung development and by cAMP and dexamethasone in fetal lung tissues in vitro. Southern hybridization analysis of genomic DNA suggested that SP-C mRNAs are encoded by a single gene. Polymerase [corrected] chain reaction-amplification of genomic DNA with oligonucleotide primers flanking the insertional sequence and sequence analysis of amplified DNA showed that SP-C mRNAs are produced by alternative use of 3' splice sites of intron 5 of SP-C gene.

scholarly journals Expression and Glucocorticoid Regulation of Surfactant Protein C in Human Fetal Lung

1997 ◽  
Vol 42 (3) ◽  
pp. 356-364 ◽  
Author(s):  
Kola O Solarin ◽  
Philip L Ballard ◽  
Susan H Guttentag ◽  
Catherine A Lomax ◽  
Michael F Beers
Keyword(s):  
Protein C ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Surfactant Protein C ◽  
Human Fetal Lung

Surfactant protein B processing in human fetal lung

1998 ◽  
Vol 275 (3) ◽  
pp. L559-L566 ◽  
Author(s):  
Susan H. Guttentag ◽  
Michael F. Beers ◽  
Bert M. Bieler ◽  
Philip L. Ballard
Keyword(s):  
Polyclonal Antibodies ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Explant Culture ◽  
Normal Lung ◽  
Surfactant Protein B ◽  
Multistep Process ◽  
Human Fetal Lung ◽  
Protein B

Surfactant protein B (SP-B8), an 8-kDa hydrophobic protein essential for surfactant and normal lung function, is produced from the intracellular processing of preproSP-B. To characterize SP-B processing in human type 2 cells, we used human fetal lung in explant culture and polyclonal antibodies to human SP-B8(Phe201–Met279) and to specific epitopes within the NH2- and COOH-terminal propeptide domains (Ser145–Leu160, Gln186–Gln200, and Gly284–Ser304). Western blot analysis revealed a novel intermediate at ∼9 kDa, representing mature SP-B8, with a residual NH2-terminal peptide of ∼10 amino acids. Pulse-chase studies showed a precursor-product relationship between the 9- and 8-kDa forms. During differentiation of type 2 cells in explant culture, the rate of proSP-B conversion to 25-kDa intermediate remained constant, whereas the rate of 25-kDa intermediate conversion to SP-B8increased, resulting in a net increase in tissue SP-B8. Dexamethasone did not affect the rate of proSP-B processing but markedly enhanced the rate of SP-B8 accumulation. We conclude that NH2-terminal propeptide cleavage of proSP-B is a multistep process and that more distal processing events are rate limiting and both developmentally and hormonally regulated.

Embryonic stem cells form glandular structures and express surfactant protein C following culture with dissociated fetal respiratory tissue

2006 ◽  
Vol 290 (6) ◽  
pp. L1210-L1215 ◽  
Author(s):  
Mark Denham ◽  
Timothy J. Cole ◽  
Richard Mollard
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Protein C ◽  
Single Cells ◽  
Cell Mass ◽  
Embryonic Stem ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Surfactant Protein C ◽  
Visceral Mesoderm

Mouse embryonic stem cells (MESCs) are pluripotent, theoretically immortal cells derived from the inner cell mass of developing blastocysts. The respiratory epithelium develops from the primitive foregut endoderm as a result of inductive morphogenetic interactions with the surrounding visceral mesoderm. After dissociation of the explanted fetal lung into single cells, these morphogenetic signaling pathways instruct reconstitution of the developing lung according to a process known as organotypic regeneration. Data presented here demonstrate that such fetal lung morphogenetic cues induce MESC derivatives to incorporate into the reforming pseudoglandular-like tubular ducts, display pan-keratin and surfactant protein C (Sftpc) immunoreactivity, and express Sftpc transcripts while displaying a normal diploid karyotype in coculture. The Sftpc inductive capacity of dissociated fetal lung tissue shows stage specificity with 24% of all MESC derivatives displaying Sftpc immunoreactivity after coculture with embryonic day 11.5 (E11.5) lung buds compared with 6% and 0.02% following coculture with E12.5 and E13.5 lung buds, respectively. MESC derivative Sftpc immunoreactivity follows a spatial and temporal specific maturation profile with an initially ubiquitous cellular Sftpc immunostaining pattern becoming apically polarized with time. Directing differentiation of MESCs into respiratory lineages has important implications for cell replacement therapeutics aimed at treating respiratory-specific diseases such as cystic fibrosis and idiopathic pulmonary fibrosis.

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