Details

Autor(en) / Beteiligte

• Cho, Hyun-Ju
• Sheen, Youn Ho
• Kang, Mi-Jin
• Lee, Seung-Hwa
• Lee, So-Yeon
• Yoon, Jisun
• Jung, Sungsu
• Lee, Si Hyeon
• Kim, Young-Ho
• Yang, Song-I
• Lee, Eun
• Seo, Ju-Hee
• Ahn, Kangmo
• Kim, Kyung Won
• Suh, Dong In
• Won, Hye-Sung
• Lee, Mi-Young
• Kim, Soo Hyun
• Choi, Suk-Joo
• Kwon, Ja-Young
• Jun, Jong Kwan
• Kwon, Sung-Ok
• Oh, Se-Young
• Hong, Soo-Jong

Titel

Prenatal 25-hydroxyvitamin D deficiency affects development of atopic dermatitis via DNA methylation

Ist Teil von

• Journal of allergy and clinical immunology, 2019-03, Vol.143 (3), p.1215-1218

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2019

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Collectively, CB 25[OH]D deficiency, as a marker of the vitD status during pregnancy, may cause a loss of methylation in the MICAL3 gene in placenta (see Fig E4 in this article's Online Repository at www.jacionline.org). Because the MICAL3 is a member of the MICAL family of flavoprotein mono-oxygenases implicated in axon guidance and actin remodeling via the oxidation of actin molecules or the production of reactive oxygen species (ROS),4 the MICAL3 overexpression-induced ROS could then overwhelm the fetal antioxidant defenses, leading to the subsequent development of AD within the first 3 years of life. [...]MICAL3 expression levels were associated with the CB 25[OH]D levels regardless of AD presence (see this article's Results section and Fig E5 in the Online Repository at www.jacionline.org). Because this was a prospective birth cohort study, it means that there was already an interaction between MICAL3 expression and CB 25[OH]D levels at birth before the development of AD. To replicate the ROS-associated AD mechanism evidenced by our study of MICAL3, we selected another gene, 8-oxoguanine DNA glycosylase (OGG1), known to impact allergic disease in association with oxidative stress for the mRNA expression data.5 Consistently, the children with AD and CB 25[OH]D deficiency had a 5.22-fold greater OGG1 mRNA expression compared with healthy subjects with CB 25[OH]D sufficiency (Fig 2, D; P = .051).