High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells
A diet high in sodium chloride (NaCl) can affect renal function damage and increase urinary calcium excretion, leading to bone loss. in renal tubules, Na-Cl co-transporter (NCC) and chloride channel 5 (CLC-5) are involved in regulating urinary calcium excretion. In addition, some cytokines, such as...
| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2021-12-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651321008745 |
| _version_ | 1818881727814172672 |
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| author | Shu Mo Yan Cui Kehuan Sun Haixia Wang Xunqian Peng Ling Ou Xiaojun Lei Mengtian Huang Wenhui Mei Ling Xin Haibing He Bojia Peng Ya Tian Panpan Wang Xiaoyun Li Ronghua Zhang Xiaofeng Zhu |
| author_facet | Shu Mo Yan Cui Kehuan Sun Haixia Wang Xunqian Peng Ling Ou Xiaojun Lei Mengtian Huang Wenhui Mei Ling Xin Haibing He Bojia Peng Ya Tian Panpan Wang Xiaoyun Li Ronghua Zhang Xiaofeng Zhu |
| author_sort | Shu Mo |
| collection | DOAJ |
| description | A diet high in sodium chloride (NaCl) can affect renal function damage and increase urinary calcium excretion, leading to bone loss. in renal tubules, Na-Cl co-transporter (NCC) and chloride channel 5 (CLC-5) are involved in regulating urinary calcium excretion. In addition, some cytokines, such as Bone morphogenetic protein 7 (BMP-7) and 1α-hydroxylase, are synthesized by renal tubules, which target on bone and play important roles on bone metabolism. However, the specific mechanisms between NaCl and these ion channels or cytokines still need investigations from many aspects. This study, in culture normal rat renal tubular epithelial NRK-52E cells, showed that high concentrations of NaCl significantly inhibited the cell viability and increased the cell apoptosis. High concentration of NaCl reduce bone mineral density (BMD), as demonstrated by the significantly increased mRNA and protein levels of NCC and osteopontin (OPN), but decreased the levels of CLC-5, BMP-7, and 1α-hydroxylase. In addition, we found that ovariectomized (OVX) rats on a high-salt diet for 12 weeks had altered levels of these indices in the renal cortices. Moreover, the BMD in fourth and fifth lumbar vertebra (LV4 and 5) and femurs were significantly decreased and bone microstructure was destroyed of these rats. We also demonstrated that high concentration of NaCl enhanced the inhibition of these cytokines which is beneficial to increase BMD, induced by modulating ion channels NCC and CLC-5. In conclusion, our results indicate that high concentration of NaCl reduce BMD by regulating ion channels NCC and CLC-5. |
| first_indexed | 2024-12-19T15:06:28Z |
| format | Article |
| id | doaj.art-b3e03bdfc1fe4504885cbb3eeb0b8814 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-12-19T15:06:28Z |
| publishDate | 2021-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-b3e03bdfc1fe4504885cbb3eeb0b88142022-12-21T20:16:26ZengElsevierEcotoxicology and Environmental Safety0147-65132021-12-01225112762High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cellsShu Mo0Yan Cui1Kehuan Sun2Haixia Wang3Xunqian Peng4Ling Ou5Xiaojun Lei6Mengtian Huang7Wenhui Mei8Ling Xin9Haibing He10Bojia Peng11Ya Tian12Panpan Wang13Xiaoyun Li14Ronghua Zhang15Xiaofeng Zhu16The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR China; College of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR China; Shenzhen Hospital of Traditional Chinese Medicine, Shenzhen, Guangdong, 518000, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Pharmacy, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Clinical Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Clinical Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Pharmacy, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Pharmacy, Jinan University, Guangzhou, Guangdong 510630, PR ChinaCollege of Pharmacy, Jinan University, Guangzhou, Guangdong 510630, PR ChinaThe First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR China; Cancer research Institution, Jinan University, Guangzhou, Guangdong, 510630, PR China; Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR China; Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, 510630, PR ChinaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR China; College of Pharmacy, Jinan University, Guangzhou, Guangdong 510630, PR China; Cancer research Institution, Jinan University, Guangzhou, Guangdong, 510630, PR China; Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, 510630, PR China; Corresponding authors at: The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR ChinaThe First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR China; Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, 510630, PR China; Corresponding authors at: The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR ChinaA diet high in sodium chloride (NaCl) can affect renal function damage and increase urinary calcium excretion, leading to bone loss. in renal tubules, Na-Cl co-transporter (NCC) and chloride channel 5 (CLC-5) are involved in regulating urinary calcium excretion. In addition, some cytokines, such as Bone morphogenetic protein 7 (BMP-7) and 1α-hydroxylase, are synthesized by renal tubules, which target on bone and play important roles on bone metabolism. However, the specific mechanisms between NaCl and these ion channels or cytokines still need investigations from many aspects. This study, in culture normal rat renal tubular epithelial NRK-52E cells, showed that high concentrations of NaCl significantly inhibited the cell viability and increased the cell apoptosis. High concentration of NaCl reduce bone mineral density (BMD), as demonstrated by the significantly increased mRNA and protein levels of NCC and osteopontin (OPN), but decreased the levels of CLC-5, BMP-7, and 1α-hydroxylase. In addition, we found that ovariectomized (OVX) rats on a high-salt diet for 12 weeks had altered levels of these indices in the renal cortices. Moreover, the BMD in fourth and fifth lumbar vertebra (LV4 and 5) and femurs were significantly decreased and bone microstructure was destroyed of these rats. We also demonstrated that high concentration of NaCl enhanced the inhibition of these cytokines which is beneficial to increase BMD, induced by modulating ion channels NCC and CLC-5. In conclusion, our results indicate that high concentration of NaCl reduce BMD by regulating ion channels NCC and CLC-5.http://www.sciencedirect.com/science/article/pii/S0147651321008745Bone mineral densityCLC-5NCCNRK-52E cellSodium chloride |
| spellingShingle | Shu Mo Yan Cui Kehuan Sun Haixia Wang Xunqian Peng Ling Ou Xiaojun Lei Mengtian Huang Wenhui Mei Ling Xin Haibing He Bojia Peng Ya Tian Panpan Wang Xiaoyun Li Ronghua Zhang Xiaofeng Zhu High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells Ecotoxicology and Environmental Safety Bone mineral density CLC-5 NCC NRK-52E cell Sodium chloride |
| title | High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells |
| title_full | High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells |
| title_fullStr | High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells |
| title_full_unstemmed | High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells |
| title_short | High sodium chloride affects BMP-7 and 1α-hydroxylase levels through NCC and CLC-5 in NRK-52E cells |
| title_sort | high sodium chloride affects bmp 7 and 1α hydroxylase levels through ncc and clc 5 in nrk 52e cells |
| topic | Bone mineral density CLC-5 NCC NRK-52E cell Sodium chloride |
| url | http://www.sciencedirect.com/science/article/pii/S0147651321008745 |
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