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Xie, Xuemei; Lin, Tulian; Zhang, Meihui; Liao, Lihong; Yuan, Guandou; Gao, Hongjie; Ning, Qin; Luo, Xiaoping

doi:10.1038/pr.2015.43

Cited by 1 publication

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“…However, positive correlations between promoter methylation and increased gene expression have been reported (Wagner et al, 2014). It was found that DNA methylation changes in nitric oxide signaling systems such as nitric oxide synthase and arginase are associated with chronic cardiopulmonary disease in adult children of IUGR (Xie et al, 2015). It should be noted that more serious asthma was developed in the IUGR mice, presenting with more significant eosinophil infiltration, mucus accumulation and inflammatory cytokines production ( Figs.…”

Section: Discussionmentioning

confidence: 96%

“…Increased phosphorylation of the insulin receptor substrate (IRS) leads to the development of insulin resistance. In addition, postnatal overnutrition in IUGR rats can upregulate DNA methylation levels at specific sites of peroxisome proliferator activated receptor γ coactivator-1α (PGC1α), promotes the development of insulin resistance, in which PI3K/Akt activity is reduced (Xie et al, 2015). Vascular noninflammatory molecule 1 (vannin-1) is a GPI-Biology Open • Accepted manuscript anchored cell surface protein encoded by the Vnn1 gene.…”

Section: Introductionmentioning

confidence: 99%

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Methylated Vnn1 at promoter regions induces asthma occurrence via the PI3K/Akt/NFκB-mediated inflammation in the IUGR mice

et al. 2020

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statementVascular noninflammatory molecule 1 (Vannin-1) is elevated in the intrauterine growth retardation (IUGR) asthmatic mice, leading to activation of the PI3K/Akt/NFκB pathway responsible for bronchial oxidative stress and hyperresponsiveness. AbstractIntrauterine growth retardation (IUGR) has high risk of developing bronchial asthma in childhood, whereas the underlying mechanisms remain unclear. This study aimed to disclose the role of vascular noninflammatory molecule 1 (vannin-1, encoded by the Vnn1 gene) and its downstream signaling in the IUGR asthmatic mice induced by ovalbumin. More significant histological alterations and increase of vannin-1 expressions were revealed in IUGR asthmatic mice, accompanied by elevated methylation of Vnn1 promoter regions. In IUGR asthmatic mice, we also found i) a direct binding of HNF4α and PGC1α to Vnn1 promoter by CHIP assay; ii) a direct interaction of HNF4α with PGC1α; iii) upregulation of phospho-PI3K p85/p55 and phospho-Akt Ser473 and downregulation of phospho-PTENT yr366 ; iv) increase in nuclear NFκB p65 and decrease in cytosolic IκB-α. In primary cultured bronchial epithelial cells derived from the IUGR asthmatic mice, knockdown of Vnn1 prevented upregulation of phospho-Akt Ser473 and increase of reactive oxygen species (ROS) and TGF-β production. Taken together, we demonstrate that elevated vannin-1 activates the PI3K/Akt/NFκB signaling pathway, leading to ROS and inflammation reactions responsible for asthma occurrence in IUGR. We also disclose that interaction of PGC1α and HNF4α promotes methylation of Vnn1 promoter regions and then upregulates vannin-1 expression.Biology Open • Accepted manuscript by guest on August 5, 2020 http://bio.biologists.org/ Downloaded from

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%