Browsing by Author "Huang, Zhiqing"
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- Association between PEG3 DNA methylation and high-grade cervical intraepithelial neoplasiaBosire, Claire; Vidal, Adriana C.; Smith, Jennifer S.; Jima, Dereje; Huang, Zhiqing; Skaar, David; Valea, Fidel; Bentley, Rex; Gradison, Margaret; Yarnall, Kimberly S. H.; Ford, Anne; Overcash, Francine; Murphy, Susan K.; Hoyo, Cathrine (2021-06-13)Background Epigenetic mechanisms are hypothesized to contribute substantially to the progression of cervical intraepithelial neoplasia (CIN) to cervical cancer, although empirical data are limited. Methods Women (n = 419) were enrolled at colposcopic evaluation at Duke Medical Center in Durham, North Carolina. Human papillomavirus (HPV) was genotyped by HPV linear array and CIN grade was ascertained by biopsy pathologic review. DNA methylation was measured at differentially methylated regions (DMRs) regulating genomic imprinting of the IGF2/H19, IGF2AS, MESTIT1/MEST, MEG3, PLAGL1/HYMAI, KvDMR and PEG10, PEG3 imprinted domains, using Sequenom-EpiTYPER assays. Logistic regression models were used to evaluate the associations between HPV infection, DMR methylation and CIN risk overall and by race. Results Of the 419 participants, 20 had CIN3+, 52 had CIN2, and 347 had ≤ CIN1 (CIN1 and negative histology). The median participant age was 28.6 (IQR:11.6) and 40% were African American. Overall, we found no statistically significant association between altered methylation in selected DMRs and CIN2+ compared to ≤CIN1. Similarly, there was no significant association between DMR methylation and CIN3+ compared to ≤CIN2. Restricting the outcome to CIN2+ cases that were HR-HPV positive and p16 staining positive, we found a significant association with PEG3 DMR methylation (OR: 1.56 95% CI: 1.03–2.36). Conclusions While the small number of high-grade CIN cases limit inferences, our findings suggest an association between altered DNA methylation at regulatory regions of PEG3 and high grade CIN in high-risk HPV positive cases.
- Blood monocyte transcriptome and epigenome analyses reveal loci associated with human atherosclerosisLiu, Yongmei; Reynolds, Lindsay M.; Ding, Jingzhong; Hou, Li; Lohman, Kurt; Young, Tracey; Cui, Wei; Huang, Zhiqing; Grenier, Carole; Wan, Ma; Stunnenberg, Hendrik G.; Siscovick, David; Hou, Lifang; Psaty, Bruce M.; Rich, Stephen S.; Rotter, Jerome I.; Kaufman, Joel D.; Burke, Gregory L.; Murphy, Susan F.; Jacobs, David R. Jr.; Post, Wendy; Hoeschele, Ina; Bell, Douglas A.; Herrington, David M.; Parks, John S.; Tracy, Russell P.; McCall, Charles E.; Stein, James H. (Springer Nature, 2017-08-30)Little is known regarding the epigenetic basis of atherosclerosis. Here we present the CD14+ blood monocyte transcriptome and epigenome signatures associated with human atherosclerosis. The transcriptome signature includes transcription coactivator, ARID5B, which is known to form a chromatin derepressor complex with a histone H3K9Me2-specific demethylase and promote adipogenesis and smooth muscle development. ARID5B CpG (cg25953130) methylation is inversely associated with both ARID5B expression and atherosclerosis, consistent with this CpG residing in an ARID5B enhancer region, based on chromatin capture and histone marks data. Mediation analysis supports assumptions that ARID5B expression mediates effects of cg25953130 methylation and several cardiovascular disease risk factors on atherosclerotic burden. In lipopolysaccharide-stimulated human THP1 monocytes, ARID5B knockdown reduced expression of genes involved in atherosclerosis-related inflammatory and lipid metabolism pathways, and inhibited cell migration and phagocytosis. These data suggest that ARID5B expression, possibly regulated by an epigenetically controlled enhancer, promotes atherosclerosis by dysregulating immunometabolism towards a chronic inflammatory phenotype.