Journal of Microbiology

Jeong Ah Jang

2 Articles

Fibroblast Growth Factor 11 Inhibits Hepatitis B Virus Gene Expression Through FXRα Suppression: Mi So Seong , Jeong Ah Jang , Ye Rim Jeong , Ye Bin Kim , Yi Yi Kyaw , Hee Jeong Kong , Jung-Hyun Lee , JaeHun Cheong; J. Microbiol. 2023;61(7): 693-702.; DOI: https://doi.org/10.1007/s12275-023-00065-1

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Fibroblast growth factor 11 (FGF11) is a member of the intracellular FGF family, which shows different signal transmission compared with other FGF superfamily members. The molecular function of FGF11 is not clearly understood. In this study, we identified the inhibitory effect of FGF11 on hepatitis B virus (HBV) gene expression through transcriptional suppression. FGF11 decreased the mRNA and protein expression of HBV genes in liver cells. While the nuclear receptor FXRα1 increased HBV promoter transactivation, FGF11 decreased the FXRα-mediated gene induction of the HBV promoter by the FXRα agonist. Reduced endogenous levels of FXRα by siRNA and the dominant negative mutant protein (aa 1–187 without ligand binding domain) of FXRα expression indicated that HBV gene suppression by FGF11 is dependent on FXRα inhibition. In addition, FGF11 interacts with FXRα protein and reduces FXRα protein stability. These results indicate that FGF11 inhibits HBV replicative expression through the liver cell-specific transcription factor, FXRα, and suppresses HBV promoter activity. Our findings may contribute to the establishment of better regimens for the treatment of chronic HBV infections by including FGF11 to alter the bile acid mediated FXR pathway.

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Research Progress on the Mechanism and Targeted Intervention of G Protein-Coupled Bile Acid Receptor 1 (GPBAR1)-Mediated “Inflammation-Apoptosis-Metabolism-Microcirculation” Regulatory Network in Hepatitis B-Associated Liver Failure
Chao Cui, Yu Sun, Kaiyue Zhang, Jingfei Shi, Kai Wang, Shuai Gao
Drug Design, Development and Therapy.2026; Volume 20: 1. CrossRef
DNA methylation and gene expression signatures for common childhood infections
Esther Herrera-Luis, Dolors Pelegrí Sisó, Marta Vidal, Katerina Margetaki, Angelos Athanasios Korakakis Pissanidis, Ruth Aguilar, Martine Vrijheid, Carlota Dobaño, Manolis Kogevinas, Marianna Karachaliou, Mariona Bustamante
Clinical Epigenetics.2026;[Epub] CrossRef

Core promoter mutation of nucleotides A1762T and G1764A of hepatitis B virus increases core promoter transactivation by hepatocyte nuclear factor 1: Mi So Seong , Hyeon Jeong Hwang , Eun Ah Jang , Jeong Ah Jang , Wah Wah Aung , Yi Yi Kyaw , JaeHun Cheong; J. Microbiol. 2022;60(10):1039-1047. Published online September 27, 2022; DOI: https://doi.org/10.1007/s12275-022-1675-1

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Abstract PDF

Hepatitis B virus (HBV) infection highly increases the risk for liver cirrhosis and hepatocellular carcinoma (HCC). The clinical manifestation of HBV infection is determined by the mutual interplay of the viral genotype, host genetic factors, mode of transmission, adaptive mutations, and environmental factors. Core promoter activation plays a critical role in the pre-genomic RNA transcription of HBV for HBV replication. The mutations of core promoter have been implicated in HCC development. We had obtained HBV genes from Myanmar HBV infectants and identified gene variations at the core promoter region. For measuring the relative transactivation activity on core promoter, we prepared the core-promoter reporter construct. Both of A1762T and G1764A mutation were consistently found in the HBV genes with hepatocellular carcinoma. The A1762T/G1764A mutation was corresponding to K130M/V131I of HBx protein. We prepared the core promoter- luciferase reporter construct containing the double A1762T/G1764A mutation and the K130M/V131I HBx protein expression construct. The A1762T/G1764A mutation highly was responsive to core promoter transactivation by HBx, regardless of HBx mutation. The A1762T/G1764A mutation newly created hepatocyte nuclear factor 1 (HNF1) responsive element. Ectopic expression of HNF1 largely increased the HBV core promoter containing A1762T/G1764A mutation. In addition, hepatic rich fatty acid, palmitic acid and oleic acid, increased K130M/V131I HBx level by core promoter activation. These results provide biological properties and clinical significance of specific HBV core promoter mutants related with HCC development.

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A Survey of HBV Core/Pre-Core Mutations in Iraqi Patients with Chronic Hepatitis
Abdulhussain Kadhim Jwaziri, Maryam Esghaei, Mohammad Hadi Karbalaie Niya, Hadi Sayah, Mohammad Hossein Razizadeh, Ali Gholami, Leila Mousavizadeh, Hossein Keyvani
Hepatitis Monthly.2023;[Epub] CrossRef
The A1762T/G1764A mutations enhance HBV replication by alternating viral transcriptome
Danli Yang, Jun Zou, Guiwen Guan, Xiaoyu Feng, Ting Zhang, Guixin Li, Hui Liu, Huiling Zheng, Jingyuan Xi, Guangxin Yu, Lizhong Dai, Fengmin Lu, Xiangmei Chen
Journal of Medical Virology.2023;[Epub] CrossRef
Clinical application value of hepatitis B virus basal core promoter 1762/1764 and GGTII and GGT in patients with HBV-DNA-positive primary liver cancer
Shunhua Qiu, Lifen Jin, Dan Yang, Dewen Zhang
Medicine.2023; 102(43): e35699. CrossRef

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