Inhibition of Autophagy Alleviates Cadmium-Induced Mouse Spleen and Human B Cells Apoptosis

Author:

Gu Jie1,Wang Yanwei1,Liu Yanmin1,Shi Meilin1,Yin Liangdong2,Hou Yongzhong1,Zhou Yang1,Chu Wong Chris Kong3,Chen Dongfeng14,Guo Zhigang5,Shi Haifeng1

Affiliation:

1. Institute of Life Sciences, Jiangsu University

2. Department of Osteology, The Third Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212000, China

3. Department of Biology, Hong Kong Baptist University, Hong Kong SAR, China

4. Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden

5. Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing, Jiangsu 210023, China

Abstract

Abstract Cadmium (Cd) is a toxic heavy metal that can accumulate and cause severe damage to many organs, such as liver, kidney, lung, etc. Cd also significantly suppresses immunity, however, the underlying mechanism involved in Cd-induced immunnotoxicity is still unclear. The present study indicated that semichronic Cd exposure (7 days) induced apoptotic damage of mouse spleen. In human Ramos B cells, Cd exposure also induced apoptosis, which was dependent on Cd-induced vacuole membrane protein 1 (VMP1) expression and autophagy. Cd-induced autophagy and apoptosis were abated when VMP1 expression was knockdown. In addition, Cd-induced VMP1 expression, autophagy, and apoptosis were dependent on the elevation of Ca2+ and reactive oxygen species (ROS). More important, Cd exposure also induced VMP1 expression and autophagy in mouse spleen tissue, and the intraperitoneal injection of the autophagy inhibitor chloroquine (CQ) into mice effectively reduced Cd-induced spleen apoptotic damage. Taken together, these results indicate Cd-induced autophagy, promotes apoptosis in immune cells, and inhibition of autophagy can alleviate Cd-induced spleen and immune cell apoptosis. This study might provide the groundwork for future studies on Cd-induced immunomodulatory effects and immune diseases.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Jiangsu Province of China

Jiangsu University for Distinguished Scholars

Publisher

Oxford University Press (OUP)

Subject

Toxicology

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