The association between the C-509T and T869C polymorphisms of TGF-β1 gene and the risk of asthma: A meta-analysis

Che, Zhen; Zhu, Xiaoxia; Yao, Cijiang; Liu, Ying; Chen, Yanyan; Cao, Jiyu; Liang, Chunmei; Lu, Youjin

doi:10.1016/j.humimm.2013.11.008

Cited by 17 publications

(8 citation statements)

References 37 publications

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“…Additionally, TGF-β1 is one of several candidate loci in the pathogenesis of asthma in addition to being highly polymorphic. The connection between the T869C and C-509T polymorphisms of the TGF-β1 gene may be a risk factor of asthma [36]. TGF-β1 expression displayed increased levels in mice with asthma, while a correlation was detected between the higher TGF-β1 ratio in the chronic group and higher collagen levels [37].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic respiratory conditions continue to plague millions of people worldwide. We aimed to elucidate the detailed mechanisms of microRNA-485 (miR-485) in airway smooth muscle cell (ASMC) proliferation and apoptosis in chronic asthmatic mice. Methods: A mouse model of chronic asthma was established. Ovalbumin was used to induce chronic asthma in the mice. The levels of transforming growth factor β (TGF-β), interleukin (IL)-4, IL-5, IL-13 and IL-17 in bronchoalveolar lavage fluid in mice were measured by enzyme-linked immunoassays (ELISAs). ASMCs were transfected with miR-485 mimic, miR-485 inhibitor and siRNA-Smurf2. The reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses were applied to detect the mRNA and protein levels of Smurf2, α-SMA, TGF-β1 and decapentaplegic homolog (Smads). The MTT assay was utilized for cell proliferation, while flow cytometry was conducted to assess cell cycle distribution and apoptosis. Results: Lower expression of miR-485 and higher expression levels of TGF-β1, IL-4, IL-5, IL-13 and IL-17 were detected in mice with chronic asthma. Smurf2 was identified as the target gene of miR-485. Upregulation of miR-485 mimic and downregulation of Smurf2 decreased expression levels of Smurf2, α-SMA, TGF-β1 and Smad3, inhibited cell proliferation and increased apoptosis, while contrary results were observed in ASMCs transfected with miR-485 inhibitor. Conclusion: Overexpressed miR-485 inhibits cell proliferation and promotes apoptosis of ASMCs through the Smurf2-mediated TGF-β/Smads signaling pathway in mice with chronic asthma.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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“…The effect of heterogeneity was also quantified by performing another measure, I 2 =100 %×(Q−df)/Q (Higgins and Thompson 2002). I 2 statistic was used to evaluate the degree of inconsistency among studies by calculating what percentage of the total variation across studies is due to heterogeneity rather than by chance (Che et al 2014), I 2 value >50 % demonstrated a statistically significant heterogeneity, and 25 % or less, 25 to 75 %, and 75 % or more are respectively used to represent low, moderate, and high degree heterogeneity (Mustafic et al 2012). In this study, heterogeneous of study design, location, and score quality subgroup were also analyzed.…”

Section: Discussionmentioning

confidence: 99%

“…Publication bias was assessed in a Begg's test; then, the degree of asymmetry was tested by Egger's test (Che et al 2014). If publication bias was proved to be existed, we would additionally apply a trim and fill method (Duval and Tweedie 2000) to make an adjustment for publication bias.…”

Section: Discussionmentioning

confidence: 99%

“…The main reason of those difference maybe a large of increased studies published in recent 3 years, and the another reason may be that we excluded some studies previously published for the same or overlapping dataset with recent studies. What's more, in the quality score assessment part, we adapted the quality scale based on Mustafic et al (2012) and from validated scales of other articles (Carracedo-Martinez et al 2010;Che et al 2014). Because case-crossover studies controlled invariant and slowly changing confounders by the design itself, there were differences of research methods between time-series study and case-crossover study; therefore, we applied the different criteria for adjustment for confounders to time series and casecrossover studies.…”

Section: Discussionmentioning

confidence: 99%

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Short-term exposure to particulate air pollution and risk of myocardial infarction: a systematic review and meta-analysis

Luo

Zhu

Yao

et al. 2015

Environ Sci Pollut Res

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A growing number of studies have associated short-term exposure to ambient particulate matter air pollution (PM) and risk of specific cardiovascular events, just as myocardial infarction (MI). However, the results of the recent studies were inconsistent; therefore, a systematic review and meta-analysis was performed. To synthetically quantify the association between short-term exposure to PM and risk of MI, a meta-analysis was conducted to combine the estimates of effect for a relationship between short-term exposure to PM10, PM2.5 (particulate matter ≤ 10 μm, 2.5 μm in diameter) and risk of MI. Electronic database searches for all relevant published studies were updated in January 2015. And, a random-effects model was performed to estimate pooled relative risk (RR) and 95 % confidence intervals (95 % CI). Thirty-one published observational epidemiological studies were identified. Risk of MI was significantly associated with per 10 μg/m(3) increment in PM10 (OR = 1.005; 95 % CI 1.001-1.008) and PM2.5 (OR = 1.022; 95 % CI 1.015-1.030). The risk of PM2.5 exposure was relatively greater than PM10. In the subgroup analysis by study design, location, quality score, and lag exposure, the results were basically consistent with the former overall results in PM2.5 but slightly changed in PM10. Short-term exposure to particulate matter (PM2.5, PM10) was a risk factor for MI, and the results further confirmed the discovery in the previous meta-analysis.

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“…Although many studies investigated the association between single nucleotide polymorphisms (SNP) in pro-inflammatory cytokine genes and asthma phenotypes (Che et al, 2014; Padron-Morales et al, 2013; Panek et al, 2014; Savenije et al, 2011; Zeyrek et al, 2008), there is only one study that focused on DA. Beghé et al (2004) studied tumor necrosis factor-α ( TNFα ) A-308G polymorphism in TDI-induced asthma but found no significant difference in frequency of this variant between cases and asymptomatic exposed subjects.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants inTNFα,TGFB1, PTGS1andPTGS2genes are associated with diisocyanate-induced asthma

Yücesoy

Kashon

Johnson³

et al. 2015

Journal of Immunotoxicology

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Diisocyanates are the most common cause of occupational asthma, but risk factors are not well defined. A case-control study was conducted to investigate whether genetic variants in inflammatory response genes (TNFα, IL1α, IL1β, IL1RN, IL10, TGFB1, ADAM33, ALOX-5, PTGS1, PTGS2 and NAG-1/GDF15) are associated with increased susceptibility to diisocyanate asthma (DA). These genes were selected based on their role in asthmatic inflammatory processes and previously reported associations with asthma phenotypes. The main study population consisted of 237 Caucasian French Canadians from among a larger sample of 280 diisocyanate-exposed workers in two groups: workers with specific inhalation challenge (SIC) confirmed DA (DA+, n = 95) and asymptomatic exposed workers (AW, n = 142). Genotyping was performed on genomic DNA, using a 5′ nuclease PCR assay. After adjusting for potentially confounding variables of age, smoking status and duration of exposure, the PTGS1 rs5788 and TGFB1 rs1800469 single nucleotide polymorphisms (SNP) showed a protective effect under a dominant model (OR = 0.38; 95% CI = 0.17, 0.89 and OR = 0.38; 95% CI = 0.18, 0.74 respectively) while the TNFα rs1800629 SNP was associated with an increased risk of DA (OR = 2.08; 95% CI = 1.03, 4.17). Additionally, the PTGS2 rs20417 variant showed an association with increased risk of DA in a recessive genetic model (OR = 6.40; 95% CI = 1.06, 38.75).These results suggest that genetic variations in TNFα, TGFB1, PTGS1 and PTGS2 genes contribute to DA susceptibility.

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The association between the C-509T and T869C polymorphisms of TGF-β1 gene and the risk of asthma: A meta-analysis

Cited by 17 publications

References 37 publications

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Short-term exposure to particulate air pollution and risk of myocardial infarction: a systematic review and meta-analysis

Genetic variants inTNFα,TGFB1, PTGS1andPTGS2genes are associated with diisocyanate-induced asthma

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