Jie Zeng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jie Zeng has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Haoyue Yu
Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education) Tianjin Medical University Tianjin China
1 shared publication - Jiangmei Wu
School of Optometry, The Hong Kong Polytechnic University
1 shared publication - Jing Zhang
School of Optometry, The Hong Kong Polytechnic University, Hong Kong, China
1 shared publication - Junkai Huang
Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin 300070, China
1 shared publication - Lizhi Hu
Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, China
1 shared publication - Mengke Sun
Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin 300070, China
1 shared publication
Latest Publications
- 15 March 2022
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 208 (6) , 1424-1433
Aberrant HO-1/NQO1–Reactive Oxygen Species–ERK Signaling Pathway Contributes to Aggravation of TPA-Induced Irritant Contact Dermatitis in Nrf2-Deficient Mice
NF-erythroid 2–related factor 2 (Nrf2) is a major transcription factor to protect cells against reactive oxygen species (ROS) and reactive toxicants. Meanwhile, Nrf2 can inhibit contact dermatitis through redox-dependent and -independent pathways. However, the underlying mechanisms of how Nrf2 mediates irritant contact dermatitis (ICD) are still unclear. In this article, we elucidated the role of Nrf2 in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced acute ICD. Our study demonstrated that the ear thickness, redness, swelling, and neutrophil infiltration were significantly increased, accompanied by increased expression of inflammatory cytokines (IL-1α, IL-1β, IL-6, etc.) and decreased expression of antioxidant genes (HO-1 and NQO1) in Nrf2 knockout mice. Moreover, ERK phosphorylation was elevated in mouse embryonic fibroblasts (MEFs) from Nrf2 knockout mouse. Inhibition of ERK significantly alleviated TPA-induced cutaneous inflammation and ROS accumulation in MEFs derived from mouse. Conversely, ROS scavenging inhibited the ERK activation and TPA-induced inflammation in MEFs. Taken together, the findings illustrate the key role of the Nrf2/ROS/ERK signaling pathway in TPA-induced acute ICD. Key Points Nrf2 deficiency aggravates inflammatory response in ICD. Nrf2 plays a critical role in ICD through the HO-1/NQO1–ROS–ERK pathway.
- 15 March 2022
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 208 (6) , 1424-1433
Aberrant HO-1/NQO1–Reactive Oxygen Species–ERK Signaling Pathway Contributes to Aggravation of TPA-Induced Irritant Contact Dermatitis in Nrf2-Deficient Mice
NF-erythroid 2–related factor 2 (Nrf2) is a major transcription factor to protect cells against reactive oxygen species (ROS) and reactive toxicants. Meanwhile, Nrf2 can inhibit contact dermatitis through redox-dependent and -independent pathways. However, the underlying mechanisms of how Nrf2 mediates irritant contact dermatitis (ICD) are still unclear. In this article, we elucidated the role of Nrf2 in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced acute ICD. Our study demonstrated that the ear thickness, redness, swelling, and neutrophil infiltration were significantly increased, accompanied by increased expression of inflammatory cytokines (IL-1α, IL-1β, IL-6, etc.) and decreased expression of antioxidant genes (HO-1 and NQO1) in Nrf2 knockout mice. Moreover, ERK phosphorylation was elevated in mouse embryonic fibroblasts (MEFs) from Nrf2 knockout mouse. Inhibition of ERK significantly alleviated TPA-induced cutaneous inflammation and ROS accumulation in MEFs derived from mouse. Conversely, ROS scavenging inhibited the ERK activation and TPA-induced inflammation in MEFs. Taken together, the findings illustrate the key role of the Nrf2/ROS/ERK signaling pathway in TPA-induced acute ICD. Key Points Nrf2 deficiency aggravates inflammatory response in ICD. Nrf2 plays a critical role in ICD through the HO-1/NQO1–ROS–ERK pathway.