2. Academic Validation
  3. Cigarette Smoke Exposure Increases Glucose-6-phosphate Dehydrogenase, Autophagy, Fibrosis, and Senescence in Kidney Cells In Vitro and In Vivo

Cigarette Smoke Exposure Increases Glucose-6-phosphate Dehydrogenase, Autophagy, Fibrosis, and Senescence in Kidney Cells In Vitro and In Vivo

  • Oxid Med Cell Longev. 2022 Mar 27;2022:5696686. doi: 10.1155/2022/5696686.
Wen-Chih Liu 1 2,  Hsiao-Chi Chuang 3 4,  Chu-Lin Chou 5 6 7 8,  Yu-Hsuan Lee 9,  Yu-Jhe Chiu 10,  Yung-Li Wang 10,  Hui-Wen Chiu 7 10 11
Affiliations

Affiliations

  • 1 Division of Nephrology, Department of Internal Medicine, Taipei Hospital, Ministry of Health and Welfare, New Taipei City, Taiwan.
  • 2 Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan.
  • 3 School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • 4 Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
  • 5 Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
  • 6 Division of Nephrology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • 7 TMU Research Center of Urology and Kidney, Taipei Medical University, Taipei, Taiwan.
  • 8 Division of Nephrology, Department of Internal Medicine, Hsin Kuo Min Hospital, Taipei Medical University, Taoyuan City, Taiwan.
  • 9 Department of Cosmeceutics, China Medical University, Taichung, Taiwan.
  • 10 Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • 11 Department of Medical Research, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
PMID: 35387262 DOI: 10.1155/2022/5696686
Abstract

Cigarette smoke (CS) is a risk factor for chronic obstructive pulmonary disease. We attempted to investigate fully the possible effects of CS on kidney cells. We found that the viability of a human kidney proximal tubular epithelial cell line (HK-2 cells) was decreased after treatment with CS extract (CSE). In particular, the effects of CSE at low concentrations did not change the expression of Apoptosis and necrosis. Furthermore, CSE increased autophagy- and fibrosis-related proteins in HK-2 cells. Senescence-related proteins and the senescence-associated secretory phenotype (SASP) increased after HK-2 cells were treated with CSE. In addition, both RNA Sequencing and gene set enrichment analysis data revealed that glucose-6-phosphate dehydrogenase (G6PD) in the Reactive Oxygen Species (ROS) pathway is responsible for the changes in CSE-treated HK-2 cells. CSE increased G6PD expression and its activity. Moreover, the inhibition of G6PD activity increased senescence in HK-2 cells. The inhibition of Autophagy reinforced senescence in the CSE-treated cells. In a mouse model of CS exposure, CS caused kidney damage, including tubular injury and glomerulosclerosis. CS increased fibrosis, Autophagy, and G6PD expression in kidney tissue sections. In conclusion, CS induced G6PD expression, Autophagy, fibrosis, and senescence in kidney cells. G6PD has a protective role in CS-induced nephrotoxicity.

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