The Methylation Patterns of a Disintegrin and Metalloproteinase 33 Gene (ADAM33) in Adult Asthma

Yang, Pei‐Jing; Li, Ruei‐Nian; Huang, Chi-Chih; Wang, Tung-Heng; Ko, Ying‐Chin; Huang, Ming‐Shyan; Wang, Tsu‐Nai

doi:10.1159/000343280

Cited by 9 publications

(4 citation statements)

References 54 publications

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“…Findings from this study suggested that TGF- β 2 suppresses expression of ADAM33 mRNA expression by chromatin modification, rather than by gene silencing through DNA methylation [36]. This was further supported by a very recent study by investigating the methylation patterns of ADAM33 in adult asthma [37]. They designed a case-control study with 50 asthmatic patients and 50 age- and sex-matched healthy controls to examine the relationship between the CpG methylation of the ADAM33 gene and asthma using bisulfite deoxyribonucleic acid modification and sequencing.…”

Section: Epigenetic Mechanisms For Adam33 In Asthmasupporting

confidence: 70%

ADAM Metallopeptidase Domain 33 (ADAM33): A Promising Target for Asthma

Tripathi

Awasthi

Gao

2014

Mediators of Inflammation

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Over the last few years, a significant progress has been made in understanding the role of a disintegrin and metalloproteinase 33 (ADAM33) in asthma. The previous observations for the association with asthma have been replicated in over 33 different population samples worldwide. We and others have performed association analysis and meta-analysis and provided further evidence that several polymorphisms in the ADAM33 are risk factors for asthma, especially in the Asian population. Further, several studies have suggested that alterations in epigenetic marks alter the patterns of DNA methylation of ADAM33 and result in potentially adverse biological effects. Finally, while the biological activities of ADAM33 are as yet unknown, ADAM33 may play a possible role in airway remodeling because of its high expression in epithelium, myo/fibroblasts, and airway smooth muscle cells (ASMCs) and its role in promoting angiogenesis and stimulating cell proliferation and differentiation. Thus, ADAM33 represents a promising target for asthma. However, further investigations are clearly needed to discover functional ADAM33 gene polymorphisms and the role of genetic/epigenetic factors in conferring genetic susceptibility to environmental exposure induced asthma as well as biological function in asthma. This, in turn, will unlock the possibility of ADAM33 as a target for asthma therapy.

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Section: Epigenetic Mechanisms For Adam33 In Asthmasupporting

confidence: 70%

ADAM Metallopeptidase Domain 33 (ADAM33): A Promising Target for Asthma

Tripathi

Awasthi

Gao

2014

Mediators of Inflammation

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“…emphasized the importance of addressing epigenetic changes in relevant target tissues [ 31 ] while DNA methylation of STAT5A and CRIP1 in airway epithelial cells distinguished asthmatic children from non-asthmatic atopics and healthy controls, these differences were not observed in PBMC. Similarly, cell-specific DNA methylation at the A disintegrin and metalloprotease 33 (ADAM33) gene promoter, which has been implicated in severe asthma, differed considerably between epithelial cells and fibroblasts and resulted in altered gene regulation [ 32 ].…”

Section: Reviewmentioning

confidence: 99%

Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD?

Krauss‐Etschmann

Meyer

Dehmel³

et al. 2015

Clin Epigenet

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Evidence is now emerging that early life environment can have lifelong effects on metabolic, cardiovascular, and pulmonary function in offspring, a concept also known as fetal or developmental programming. In mammals, developmental programming is thought to occur mainly via epigenetic mechanisms, which include DNA methylation, histone modifications, and expression of non-coding RNAs. The effects of developmental programming can be induced by the intrauterine environment, leading to intergenerational epigenetic effects from one generation to the next. Transgenerational epigenetic inheritance may be considered when developmental programming is transmitted across generations that were not exposed to the initial environment which triggered the change. So far, inter- and transgenerational programming has been mainly described for cardiovascular and metabolic disease risk. In this review, we discuss available evidence that epigenetic inheritance also occurs in respiratory diseases, using asthma and chronic obstructive pulmonary disease (COPD) as examples. While multiple epidemiological as well as animal studies demonstrate effects of ‘toxic’ intrauterine exposure on various asthma-related phenotypes in the offspring, only few studies link epigenetic marks to the observed phenotypes. As epigenetic marks may distinguish individuals most at risk of later disease at early age, it will enable early intervention strategies to reduce such risks. To achieve this goal further, well designed experimental and human studies are needed.

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“…This led to a hypothesis that the different methylation level was related to the severity of allergic asthma, thus making it a future therapeutic and diagnostic target. Nevertheless, although ADAM 33 is identified as a factor underlying asthma exacerbation [138], there was not a considerable difference in peripheral blood leukocytes CpG methylation of the exon 9 of this gene between asthmatic adults and controls [139]. In a study by Cosio et al [140], both mild and severe asthma patients witnessed declined HDAC and augmented HAT activities in PBMC derived alveolar macrophages.…”

Section: Epigenetic Differentiation Studiesmentioning

confidence: 98%

A review of epigenetic changes in asthma: methylation and acetylation

et al. 2021

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Several studies show that childhood and adulthood asthma and its symptoms can be modulated through epigenetic modifications. Epigenetic changes are inheritable modifications that can modify the gene expression without changing the DNA sequence. The most common epigenetic alternations consist of DNA methylation and histone modifications. How these changes lead to asthmatic phenotype or promote the asthma features, in particular by immune pathways regulation, is an understudied topic. Since external effects, like exposure to tobacco smoke, air pollution, and drugs, influence both asthma development and the epigenome, elucidating the role of epigenetic changes in asthma is of great importance. This review presents available evidence on the epigenetic process that drives asthma genes and pathways, with a particular focus on DNA methylation, histone methylation, and acetylation. We gathered and assessed studies conducted in this field over the past two decades. Our study examined asthma in different aspects and also shed light on the limitations and the important factors involved in the outcomes of the studies. To date, most of the studies in this area have been carried out on DNA methylation. Therefore, the need for diagnostic and therapeutic applications through this molecular process calls for more research on the histone modifications in this disease.

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The Methylation Patterns of a Disintegrin and Metalloproteinase 33 Gene (ADAM33) in Adult Asthma

Cited by 9 publications

References 54 publications

ADAM Metallopeptidase Domain 33 (ADAM33): A Promising Target for Asthma

ADAM Metallopeptidase Domain 33 (ADAM33): A Promising Target for Asthma

Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD?

A review of epigenetic changes in asthma: methylation and acetylation

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