IndraLab
Statements
sparser
"While it is unclear whether these mechanisms operate pre- and/or perinatally, detection of the relationship between SMAD3 methylation and IL-1β production selectively among children of asthmatic mothers implies that the in utero environment is critical for directing the epigenetic trajectory towards childhood asthma."
sparser
"Notably, we also reported that stimulating normal pulmonary fibroblasts with cigarette smoke condensate in culture was sufficient to time- and dose-dependently increase the promoter methylation of SMAD3 but not that of its closely related homolog SMAD2 [ xref ], as summarized in xref A–C. Although the underlying mechanisms of the selective SMAD3 hypermethylation remains unclear, it is conceivable that the common DNMT1 increase in smokers may be involved."
sparser
"Of the large number of DNA methylation changes they identified, increased methylation in SMAD3 was: (1) associated with childhood asthma risk, a result that was replicated in two independent cohorts; (2) was the most connected node within the network of asthma-associated DMRs; and (3) was strongly and positively associated with neonatal production of IL-1β, an innate inflammatory mediator."
sparser
"Bisulfite sequencing of cord blood cell DNA from our IIS neonates and two replication cohorts (The Manchester Asthma and Allergy Study, and the Childhood Origins of ASThma Study) showed that SMAD3 promoter methylation at birth was selectively and significantly increased in asthmatic children of asthmatic mothers and was associated with childhood asthma risk."
sparser
"In addition, combining SMAD3 with other hypomethylated genes, such as ACOT7 , RASA3 , B3GNTL1 , PIGB , MAP3K5 , LPIN1 , and MYBPC3 , which are potential biomarkers of CRC in the analytical model, may improve accuracy, increase sensitivity, and reduce false-positive results when predicting CRC in circulating methylated SMAD3 ."
sparser
"Fetal epigenetic regulation is modifiable by the maternal environment and has been proposed as a mechanism by which prenatal environmental stimuli contribute to the development of respiratory disorders. xref In support of this notion, mechanistic animal studies have demonstrated that maternal microbial exposures, through DNA methylation and histone modifications, may modulate the expression of important immune factors such as interleukin (IL-4) and interferon-γ genes in the offspring’s lungs. xref , xref Increases in histone H3 acetylation linked to an asthma phenotype have been also identified in mice pups after maternal nicotine exposure. xref In humans, epigenetic modifications (e.g., SMAD3 methylation) have been proposed as a mechanism mediating the intergenerational risk of asthma in children from asthmatic mothers. xref Furthermore, epigenetic modifications may also mediate the effect of noninheritable prenatal factors on respiratory outcomes."
sparser
"Previously, we conducted a preliminary screening analysis of whole-genome methylation in 4 cases of Uygur PBL and 4 Uygur pigeon breeders without this disease using the Illumina 450K method (Illumina 450K Infinium Methylation BeadChip; SHBIO, Shanghai, China), and the results showed abnormal methylation of the Smad3 gene among the Uygur PBL patients."
sparser
"The distributions of SMAD3 methylation and log IL-1β production in non-asthmatic and asthmatic children without and with a maternal history of asthma were compared by dividing mean percentage SMAD3 methylation and log IL-1β secretion at the median, thereby creating four groups (low/low, low/high, high/low and high/high)."
sparser
"When the relation between SMAD3 methylation at birth and childhood asthma was examined separately in children with and without maternal asthma, SMAD3 methylation was found to be significantly increased in asthmatic compared to non-asthmatic children of asthmatic mothers ( P =0.005 by Wilcoxon two-sample test)."
sparser
"Our results also support that smoking and/or the anatomic location of SCC in the proximal airways, which are more exposed to cigarette smoke particles, may prime SCC-TAFs to stronger SMAD3 epigenetic repression, since cigarette smoke condensate selectively increased SMAD3 promoter methylation."