Impacts of Lipopolysaccharide on Fetal Lung Developmental Maturity and Surfactant Protein B and Surfactant Protein C Protein Expression in Gestational Diabetes Mellitus Rats

Aims: This study was conducted to investigate the relationship between a genetic polymorphism and the expression of melatonin receptor 1B (MTNR1B) in the placenta of Han Chinese women with gestational diabetes mellitus (GDM). Methods: In this study, 215 patients with GDM and 243 healthy controls were genotyped using direct sequencing for the MTNR1B single-nucleotide polymorphism rs10830963. The expression of MTNR1B in placenta was detected by immunohistochemistry and Western blotting. The association of rs10830963 with the expression of MTNR1B, plasma glucose, and insulin levels as well as blood lipid levels was investigated. Results: The genotype and allele frequencies of rs10830963 were significantly different between women with GDM and controls ( P < .05). Fasting blood glucose, fasting insulin, and homeostasis model assessment for insulin resistance in women with GDM with the GG and GC genotypes were significantly higher than those with the CC genotype ( P < .05). The expression level of MTNR1B in placenta was significantly higher in the GDM group than in the control group ( P < .05). The expression of MTNR1B was significantly higher in all participants with the GG and GC genotypes (1.31 [0.74]) than in pregnant women with the CC genotype (0.92 [0.52], P < .05). Conclusions: The genetic polymorphism rs10830963 in MTNR1B and its protein expression levels in placenta are associated with an increased risk of developing GDM. Furthermore, rs10830963 may tag a molecular mechanism leading to insulin resistance in Han Chinese women with GDM.

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Surfactant Protein D Gene Polymorphism was Associated with the Susceptibility of Gestational Diabetes Mellitus: A Case Control Study

10.21203/rs.3.rs-515102/v1 ◽

2021 ◽

Author(s):

Jingwei Xu ◽

Yi Chen ◽

Liangfang Tang ◽

Xinyuan Teng ◽

Lin Feng ◽

...

Keyword(s):

Diabetes Mellitus ◽

Gestational Diabetes ◽

Gene Polymorphism ◽

Gestational Diabetes Mellitus ◽

Gene Polymorphisms ◽

Surfactant Protein ◽

Surfactant Protein D ◽

Coding Region ◽

Increased Risk ◽

Relationship Of

Abstract BackgroundSurfactant protein D (SP-D) is a critical component of the innate immune system intrinsically linked to energetic metabolism. However, the relationship of SP-D gene polymorphisms and gestational diabetes mellitus (GDM) remains unclear yet. In this study, we analyzed SP-D gene polymorphisms in GDM patients and non-diabatic controls, and then determined the association of SP-D gene polymorphisms with GDM.MethodsWe examined a common genetic polymorphism located in the SP-D coding region (rs721917, Met31Thr) with GDM patients (n = 147) and healthy pregnant controls (n = 97) by using a PCR-RFLP technique. The level of SP-D protein in serum of GDM patients and non-diabetic controls was determined by ELISA method. The gene and allele frequencies od SP-D and their association with GDM as well as SP-D protein level were analyzed using SPSS software.ResultsWe found that there exists a significant association of the SP-D polymorphism (rs721917) with GDM. SP-D (T/T) genotype had 11.6% and 21.6% in GDM and matched healthy controls, respectively (P<0.05); indicating women with (T/T) genotype have lower prevalence of GDM (OR = 0.473). Women with T/C genotypes showed an increased risk of GDM (OR = 2.440). We did not observe corrections between glucose homeostasis markers and SP-D genotypes in the women patients with GDM. Furthermore, serum SP-D level was higher in the GDM compared to matched healthy controls.ConclusionsThis study has found the first evidence that SP-D gene polymorphism (rs721917) was associated with GDM, which may provide the basis for further study how SP-D plays a regulatory role in GDM.

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00427.2005 ◽

2006 ◽

Vol 290 (6) ◽

pp. L1210-L1215 ◽

Cited By ~ 34

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1992.263.6.l634 ◽

1992 ◽

Vol 263 (6) ◽

pp. L634-L644 ◽

Cited By ~ 6

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.

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