Exposure to airborne particulate matter induces renal tubular cell injury in vitro: The role of vitamin D signaling and renin-angiotensin systemopen access
- Authors
- Kang, Eungu; Yim, Hyung Eun; Nam, Yoon Jeong; Jeong, Sang Hoon; Kim, Joo-Ae; Lee, Ju-Han; Son, Min Hwa; Yoo, Kee Hwan
- Issue Date
- 8월-2022
- Publisher
- ELSEVIER SCI LTD
- Keywords
- Airborne Particulate Matter; Kidney Tubules; Renin-Angiotensin System; Vitamin D Deficiency
- Citation
- HELIYON, v.8, no.8
- Indexed
- SCIE
SCOPUS
- Journal Title
- HELIYON
- Volume
- 8
- Number
- 8
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/145543
- DOI
- 10.1016/j.heliyon.2022.e10184
- ISSN
- 2405-8440
- Abstract
- Background: Exposure to air pollution can interfere with the vitamin D endocrine system. This study investigated the effects of airborne particulate matter (PM) on renal tubular cell injury in vitro and explored the underlying mechanisms.Methods: HK-2 human renal proximal tubule cells were treated with PM with or without 1,25(OH)2D3 analog, 19-Nor-1,25(OH)2D2 (paricalcitol, 10 nM) for 48 hours. The dose-and time -dependent cytotoxicity of PM with or without paricalcitol was determined via cell counting kit-8 assay. Cellular oxidative stress was assessed using commercially available enzyme-linked immunosorbent assay kits. The protein expression of vitamin D receptor (VDR), cytochrome P450(CYP)27B1, CYP24A1, renin, angiotensin converting enzyme (ACE), angiotensin II type 1 receptor (AT1), nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear factor-kB (NF-kB), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-6 was determined.Results: PM exposure decreased HK-2 cell viability in a dose-and time-dependent manner. The activities of superoxide dismutase and malondialdehyde in HK-2 cells increased significantly in the group exposed to PM. PM exposure decreased VDR and Nrf2, while increasing CYP27B1, renin, ACE, AT1, NF-kB, TNF-alpha, and IL-6. The expression of VDR, CYP27B1, renin, ACE, AT1, and TNF-alpha was reversed by paricalcitol treatment. Paricalcitol also restored the cell viability of PM-exposed HK-2 cells.Conclusion: Our findings indicate that exposure to PM induces renal proximal tubular cell injury, concomitant with alteration of vitamin D endocrine system and renin angiotensin system. Vitamin D could attenuate renal tubular cell damage following PM exposure by suppressing the renin-angiotensin system and by partially inhibiting the inflammatory response.
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