Plasma Surfactant Protein D Levels and the Relation to Body Mass Index in a Chinese Population

Zhao, Xiongce; Wu, Ya Ping; Wei, Ran; Cai, Hao; Tornøe, Ida; Han, Jinmin; Wang, Y; Groot, Philip G. de; Holmskov, Uffe; Xia, Zuo Li; Sørensen, Grith Lykke

doi:10.1111/j.1365-3083.2007.01943.x

Cited by 24 publications

(25 citation statements)

References 28 publications

(35 reference statements)

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“…As shown in Table 6, age (Beta = 0.36, p < 0.001), and steroid intake (Beta = −0.36, p < 0.001) and rs3088308 influence serum SP-D levels (Beta = −0.33, p < 0.001) along with exacerbation status (Beta = 0.28, p = 0.01), body mass index (Beta = −0.26, p = 0.01) and SNP rs721917 (Beta = −0.21, p = 0.03). Our study supports the previous studies correlating age [29], body mass index [31,32], corticosteroid intake [33] and rs721917 [29,31,39] with systemic SP-D levels. We have previously reported on significantly raised serum SP-D levels in COPD exacerbations [34].…”

Section: Discussionsupporting

confidence: 82%

SP-D Polymorphisms and the Risk of COPD

et al. 2012

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Abstract.Introduction: There are limited data linking serum levels of surfactant protein D, its genetic polymorphisms to the risk of Chronic Obstructive Pulmonary Disease (COPD). Objectives: We sought to investigate these relationships using a case control study design. Methods: Post bronchodilator values of FEV1/FVC <0.7 were used to diagnose COPD patients (n = 115). Controls were healthy subjects with normal spirometry (n = 106) Single nucleotide polymorphisms (rs721917, rs2243639, rs3088308) were genotyped using polymerase chain reaction (PCR) and restriction analysis. Serum SP-D levels were measured using a specific immunoassay. Results: Allele 'A' at rs3088308 (p < 0.00, B = −0.41) and 'C' allele at rs721917 (p = 0.03; B = −0.30) were associated with reduced serum SP-D levels. Genotype 'T/T' at rs721917 was significantly associated with risk of COPD (p = 0.01). Patients with repeat exacerbations had significantly higher serum SP-D even after adjusting for genetic factors. Conclusions: We report for the first time that rs3088308 is an important factor influencing systemic SP-D levels and confirm the previous association of rs721917 to the risk of COPD and serum SP-D levels.

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Section: Discussionsupporting

confidence: 82%

SP-D Polymorphisms and the Risk of COPD

et al. 2012

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“…A possible metabolic role of SP-D is suggested by the observation that SP-D impacts systemic lipid levels and atherosclerosis (Sørensen et al 2006b). Consistent with that is the observation that circulating SP-D levels are inversely associated with obesity in humans (Zhao et al 2007). Furthermore, mice with a null mutation of the SP-D gene maintained on a normal diet exhibited more weight gain and increased adiposity compared with control mice (Sørensen et al 2006a).…”

Section: Discussionsupporting

confidence: 56%

Regulation of pancreatic islet gene expression in mouse islets by pregnancy

Layden

Durai²,

Newman³

et al. 2010

Journal of Endocrinology

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Pancreatic b cells adapt to pregnancy-induced insulin resistance by unclear mechanisms. This study sought to identify genes involved in b cell adaptation during pregnancy. To examine changes in global RNA expression during pregnancy, murine islets were isolated at a time point of increased b cell proliferation (E13 . 5), and RNA levels were determined by two different assays (global gene expression array and G-protein-coupled receptor (GPCR) array). Follow-up studies confirmed the findings for select genes. Differential expression of 110 genes was identified and follow-up studies confirmed the changes in select genes at both the RNA and protein level. Surfactant protein D (SP-D) mRNA and protein levels exhibited large increases, which were confirmed in murine islets. Cytokine-induced expression of SP-D in islets was also demonstrated, suggesting a possible role as an anti-inflammatory molecule. Complementing these studies, an expression array was performed to define pregnancy-induced changes in expression of GPCRs that are known to impact islet cell function and proliferation. This assay, the results of which were confirmed using realtime reverse transcription-PCR assays, demonstrated that free fatty acid receptor 2 and cholecystokinin receptor A mRNA levels were increased at E13 . 5. This study has identified multiple novel targets that may be important for the adaptation of islets to pregnancy.

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“…According to a mechanism postulated to explain this discordance, inflammation in the lungs of patients with COPD results in the endothelial leakage of SP-D systemically, although other mechanisms may exist (46). In addition to its potential as a lung-specific biomarker, SP-D was correlated with body mass index (BMI) (47,48). In a murine model, the overexpression of SFTPD was associated with atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in Surfactant Protein–D Are Associated with Chronic Obstructive Pulmonary Disease

Foreman¹,

Kong²,

DeMeo³

et al. 2011

Am J Respir Cell Mol Biol

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Chronic obstructive pulmonary disease (COPD) is characterized by alveolar destruction and abnormal inflammatory responses to noxious stimuli. Surfactant protein-D (SFTPD) is immunomodulatory and essential to host defense. We hypothesized that polymorphisms in SFTPD could influence the susceptibility to COPD. We genotyped six single-nucleotide polymorphisms (SNPs) in surfactant protein D in 389 patients with COPD in the National Emphysema Treatment Trial (NETT) and 472 smoking control subjects from the Normative Aging Study (NAS). Case-control association analysis was performed using Cochran-Armitage trend tests and multivariate logistic regression. The replication of significant associations was attempted in the Boston Early-Onset COPD Study, the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) Study, and the Bergen Cohort. We also correlated SFTPD genotypes with serum concentrations of surfactant protein-D (SP-D) in the ECLIPSE Study. In the NETT-NAS case-control analysis, four SFTPD SNPs were associated with susceptibility to COPD: rs2245121 (P 5 0.01), rs911887 (P 5 0.006), rs6413520 (P 5 0.004), and rs721917 (P 5 0.006). In the family-based analysis of the Boston Early-Onset COPD Study, rs911887 was associated with prebronchodilator and postbronchodilator FEV 1 (P 5 0.003 and P 5 0.02, respectively). An intronic SNP in SFTPD, rs7078012, was associated with COPD in the ECLIPSE Study and the Bergen Cohort. Multiple SFTPD SNPs were associated with serum SP-D concentrations in the ECLIPSE Study. We demonstrated an association of polymorphisms in SFTPD with COPD in multiple populations. We demonstrated a correlation between SFTPD SNPs and SP-D protein concentrations. The SNPs associated with COPD and SP-D concentrations differed, suggesting distinct genetic influences on susceptibility to COPD and SP-D concentrations.

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Plasma Surfactant Protein D Levels and the Relation to Body Mass Index in a Chinese Population

Cited by 24 publications

References 28 publications

SP-D Polymorphisms and the Risk of COPD

SP-D Polymorphisms and the Risk of COPD

Regulation of pancreatic islet gene expression in mouse islets by pregnancy

Polymorphisms in Surfactant Protein–D Are Associated with Chronic Obstructive Pulmonary Disease

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