Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy

Rui Li; Qingfen Wang; Xiaochun Niu; Ruirui Xu

doi:doi:10.11648/j.ajcem.20180605.12

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Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy

Rui Li, Qingfen Wang, Xiaochun Niu, Ruirui Xu

Published in American Journal of Clinical and Experimental Medicine (Volume 6, Issue 5)

Received: 5 December 2018 Published: 6 December 2018

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Abstract

To observe the effect of high glucose stimulation on the expression of guanylate exchange factor NHX1 in mouse kidney cells, and to explore the role of NHX1 in high glucose-induced podocyte injury and its possible molecular mechanism. The expression of NHX1 in podocytes of diabetic nephropathy patients was observed by immunofluorescence staining and laser confocal microscopy. The immortalized podocytes were cultured in vitro, and the podocytes were stimulated with high glucose for 48 h. RT-PCR, Western blot and immunization were used. Fluorescence detection of mRNA and protein expression of NHX1 in podocytes stimulated by high glucose; Western blot, immunofluorescence and scratch assay were used to detect the expression of NHX1 and the expression of podocin, the activity of podocytes and the nuclear access of TRPV5. The transcription of the target gene downstream of TRPV5 was detected by RT-PCR. NHX1 expression was significantly decreased in podocytes and high glucose-stimulated podocytes of diabetic nephropathy patients (P<0.05). After silencing NHX1, podocyte marker protein podocin expression was significantly decreased and podocyte activity was increased. The nuclear translocation of TRPV5 increased, and the transcription of the target gene downstream of TRPV5 increased (P < 0.05). In contrast, the expression of overexpressed NHX1 group was significantly increased, the activity of podocytes was decreased, the nuclear access of TRPV5 was decreased, and the transcription of the target gene downstream of TRPV5 was decreased (P<0.05). NHX1 may reduce podocyte injury in diabetic nephropathy by inhibiting TRPV5 entry into the nucleus.

Published in	American Journal of Clinical and Experimental Medicine (Volume 6, Issue 5)
DOI	10.11648/j.ajcem.20180605.12
Page(s)	113-117
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2018. Published by Science Publishing Group

Keywords

Diabetic Nephropathy, Podocyte, NHX1 Protein, TRPV5 Protein

References

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[2]	Chen X, Zhao L, Xing Y, Lin B. Down-regulation of microRNA-21 reduces inflammation and podocyte apoptosis in diabetic nephropathy by relieving the repression of TIMP3 expression. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2018; 108: 7-14.
[3]	Zhong F, Chen H, Xie Y, Azeloglu EU, Wei C, Zhang W, et al. Protein S Protects against Podocyte Injury in Diabetic Nephropathy. Journal of the American Society of Nephrology: JASN. 2018; 29 (5): 1397-410.
[4]	Bai X, Geng J, Li X, Wan J, Liu J, Zhou Z, et al. Long Noncoding RNA LINC01619 Regulates MicroRNA-27a/Forkhead Box Protein O1 and Endoplasmic Reticulum Stress-Mediated Podocyte Injury in Diabetic Nephropathy. Antioxidants & redox signaling. 2018; 29 (4): 355-76.
[5]	Fujita Y, Tominaga T, Abe H, Kangawa Y, Fukushima N, Ueda O, et al. An adjustment in BMP4 function represents a treatment for diabetic nephropathy and podocyte injury. Scientific reports. 2018; 8 (1): 13011.
[6]	Zhang Z, Li X, Liu L, Sun J, Wang X, Zhao Z, et al. Tiaolipiwei Acupuncture Reduces Albuminuria by Alleviating Podocyte Lesions in a Rat Model of Diabetic Nephropathy. Evidence-based complementary and alternative medicine: eCAM. 2018; 2018: 1913691.
[7]	He Y, Zhang M, Wu Y, Jiang H, Fu H, Cai Y, et al. Aberrant activation of Notch-1 signaling inhibits podocyte restoration after islet transplantation in a rat model of diabetic nephropathy. Cell death & disease. 2018; 9 (10): 950.
[8]	Zhang Y, Chen X, Yuan L, Wu J, Guo N, Liu J. Down-regulation of IRAK1 attenuates podocyte apoptosis in diabetic nephropathy through PI3K/Akt signaling pathway. Biochemical and biophysical research communications. 2018; 506 (3): 529-35.
[9]	Lei X, Zhang L, Li Z, Ren J. Astragaloside IV/lncRNA-TUG1/TRAF5 signaling pathway participates in podocyte apoptosis of diabetic nephropathy rats. Drug design, development and therapy. 2018; 12: 2785-93.
[10]	Wang Y, Li H, Song SP. beta-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/beta-Catenin Pathway. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 1724-32.
[11]	Pan Y, Jiang S, Hou Q, Qiu D, Shi J, Wang L, et al. Dissection of Glomerular Transcriptional Profile in Patients With Diabetic Nephropathy: SRGAP2a Protects Podocyte Structure and Function. Diabetes. 2018; 67 (4): 717-30.
[12]	Wang XB, Zhu H, Song W, Su JH. Gremlin Regulates Podocyte Apoptosis via Transforming Growth Factor-beta (TGF-beta) Pathway in Diabetic Nephropathy. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 183-9.
[13]	Lv Z, Hu M, Fan M, Li X, Lin J, Zhen J, et al. Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice. Cell death & disease. 2018; 9 (3): 342.
[14]	Wang X, Gao L, Lin H, Song J, Wang J, Yin Y, et al. Mangiferin prevents diabetic nephropathy progression and protects podocyte function via autophagy in diabetic rat glomeruli. European journal of pharmacology. 2018; 824: 170-8.
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APA Style

Rui Li, Qingfen Wang, Xiaochun Niu, Ruirui Xu. (2018). Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. American Journal of Clinical and Experimental Medicine, 6(5), 113-117. https://doi.org/10.11648/j.ajcem.20180605.12

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ACS Style

Rui Li; Qingfen Wang; Xiaochun Niu; Ruirui Xu. Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. Am. J. Clin. Exp. Med. 2018, 6(5), 113-117. doi: 10.11648/j.ajcem.20180605.12

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AMA Style

Rui Li, Qingfen Wang, Xiaochun Niu, Ruirui Xu. Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. Am J Clin Exp Med. 2018;6(5):113-117. doi: 10.11648/j.ajcem.20180605.12

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@article{10.11648/j.ajcem.20180605.12,
  author = {Rui Li and Qingfen Wang and Xiaochun Niu and Ruirui Xu},
  title = {Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {6},
  number = {5},
  pages = {113-117},
  doi = {10.11648/j.ajcem.20180605.12},
  url = {https://doi.org/10.11648/j.ajcem.20180605.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20180605.12},
  abstract = {To observe the effect of high glucose stimulation on the expression of guanylate exchange factor NHX1 in mouse kidney cells, and to explore the role of NHX1 in high glucose-induced podocyte injury and its possible molecular mechanism. The expression of NHX1 in podocytes of diabetic nephropathy patients was observed by immunofluorescence staining and laser confocal microscopy. The immortalized podocytes were cultured in vitro, and the podocytes were stimulated with high glucose for 48 h. RT-PCR, Western blot and immunization were used. Fluorescence detection of mRNA and protein expression of NHX1 in podocytes stimulated by high glucose; Western blot, immunofluorescence and scratch assay were used to detect the expression of NHX1 and the expression of podocin, the activity of podocytes and the nuclear access of TRPV5. The transcription of the target gene downstream of TRPV5 was detected by RT-PCR. NHX1 expression was significantly decreased in podocytes and high glucose-stimulated podocytes of diabetic nephropathy patients (P<0.05). After silencing NHX1, podocyte marker protein podocin expression was significantly decreased and podocyte activity was increased. The nuclear translocation of TRPV5 increased, and the transcription of the target gene downstream of TRPV5 increased (P < 0.05). In contrast, the expression of overexpressed NHX1 group was significantly increased, the activity of podocytes was decreased, the nuclear access of TRPV5 was decreased, and the transcription of the target gene downstream of TRPV5 was decreased (P<0.05). NHX1 may reduce podocyte injury in diabetic nephropathy by inhibiting TRPV5 entry into the nucleus.},
 year = {2018}
}

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TY  - JOUR
T1  - Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy
AU  - Rui Li
AU  - Qingfen Wang
AU  - Xiaochun Niu
AU  - Ruirui Xu
Y1  - 2018/12/06
PY  - 2018
N1  - https://doi.org/10.11648/j.ajcem.20180605.12
DO  - 10.11648/j.ajcem.20180605.12
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 113
EP  - 117
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20180605.12
AB  - To observe the effect of high glucose stimulation on the expression of guanylate exchange factor NHX1 in mouse kidney cells, and to explore the role of NHX1 in high glucose-induced podocyte injury and its possible molecular mechanism. The expression of NHX1 in podocytes of diabetic nephropathy patients was observed by immunofluorescence staining and laser confocal microscopy. The immortalized podocytes were cultured in vitro, and the podocytes were stimulated with high glucose for 48 h. RT-PCR, Western blot and immunization were used. Fluorescence detection of mRNA and protein expression of NHX1 in podocytes stimulated by high glucose; Western blot, immunofluorescence and scratch assay were used to detect the expression of NHX1 and the expression of podocin, the activity of podocytes and the nuclear access of TRPV5. The transcription of the target gene downstream of TRPV5 was detected by RT-PCR. NHX1 expression was significantly decreased in podocytes and high glucose-stimulated podocytes of diabetic nephropathy patients (P<0.05). After silencing NHX1, podocyte marker protein podocin expression was significantly decreased and podocyte activity was increased. The nuclear translocation of TRPV5 increased, and the transcription of the target gene downstream of TRPV5 increased (P < 0.05). In contrast, the expression of overexpressed NHX1 group was significantly increased, the activity of podocytes was decreased, the nuclear access of TRPV5 was decreased, and the transcription of the target gene downstream of TRPV5 was decreased (P<0.05). NHX1 may reduce podocyte injury in diabetic nephropathy by inhibiting TRPV5 entry into the nucleus.
VL  - 6
IS  - 5
ER  -

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Author Information

Rui Li

Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Qingfen Wang

Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Xiaochun Niu

Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Ruirui Xu

Department of Nephrology, Binzhou People's Hospital, Binzhou, China

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APA Style

Rui Li, Qingfen Wang, Xiaochun Niu, Ruirui Xu. (2018). Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. American Journal of Clinical and Experimental Medicine, 6(5), 113-117. https://doi.org/10.11648/j.ajcem.20180605.12

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ACS Style

Rui Li; Qingfen Wang; Xiaochun Niu; Ruirui Xu. Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. Am. J. Clin. Exp. Med. 2018, 6(5), 113-117. doi: 10.11648/j.ajcem.20180605.12

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AMA Style

Rui Li, Qingfen Wang, Xiaochun Niu, Ruirui Xu. Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy. Am J Clin Exp Med. 2018;6(5):113-117. doi: 10.11648/j.ajcem.20180605.12

Copy | Download

@article{10.11648/j.ajcem.20180605.12,
  author = {Rui Li and Qingfen Wang and Xiaochun Niu and Ruirui Xu},
  title = {Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {6},
  number = {5},
  pages = {113-117},
  doi = {10.11648/j.ajcem.20180605.12},
  url = {https://doi.org/10.11648/j.ajcem.20180605.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20180605.12},
  abstract = {To observe the effect of high glucose stimulation on the expression of guanylate exchange factor NHX1 in mouse kidney cells, and to explore the role of NHX1 in high glucose-induced podocyte injury and its possible molecular mechanism. The expression of NHX1 in podocytes of diabetic nephropathy patients was observed by immunofluorescence staining and laser confocal microscopy. The immortalized podocytes were cultured in vitro, and the podocytes were stimulated with high glucose for 48 h. RT-PCR, Western blot and immunization were used. Fluorescence detection of mRNA and protein expression of NHX1 in podocytes stimulated by high glucose; Western blot, immunofluorescence and scratch assay were used to detect the expression of NHX1 and the expression of podocin, the activity of podocytes and the nuclear access of TRPV5. The transcription of the target gene downstream of TRPV5 was detected by RT-PCR. NHX1 expression was significantly decreased in podocytes and high glucose-stimulated podocytes of diabetic nephropathy patients (P<0.05). After silencing NHX1, podocyte marker protein podocin expression was significantly decreased and podocyte activity was increased. The nuclear translocation of TRPV5 increased, and the transcription of the target gene downstream of TRPV5 increased (P < 0.05). In contrast, the expression of overexpressed NHX1 group was significantly increased, the activity of podocytes was decreased, the nuclear access of TRPV5 was decreased, and the transcription of the target gene downstream of TRPV5 was decreased (P<0.05). NHX1 may reduce podocyte injury in diabetic nephropathy by inhibiting TRPV5 entry into the nucleus.},
 year = {2018}
}

Copy | Download

TY  - JOUR
T1  - Mechanism of NHX1 Inhibiting TRPV5-Mediated Podocyte Injury in Diabetic Nephropathy
AU  - Rui Li
AU  - Qingfen Wang
AU  - Xiaochun Niu
AU  - Ruirui Xu
Y1  - 2018/12/06
PY  - 2018
N1  - https://doi.org/10.11648/j.ajcem.20180605.12
DO  - 10.11648/j.ajcem.20180605.12
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 113
EP  - 117
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20180605.12
AB  - To observe the effect of high glucose stimulation on the expression of guanylate exchange factor NHX1 in mouse kidney cells, and to explore the role of NHX1 in high glucose-induced podocyte injury and its possible molecular mechanism. The expression of NHX1 in podocytes of diabetic nephropathy patients was observed by immunofluorescence staining and laser confocal microscopy. The immortalized podocytes were cultured in vitro, and the podocytes were stimulated with high glucose for 48 h. RT-PCR, Western blot and immunization were used. Fluorescence detection of mRNA and protein expression of NHX1 in podocytes stimulated by high glucose; Western blot, immunofluorescence and scratch assay were used to detect the expression of NHX1 and the expression of podocin, the activity of podocytes and the nuclear access of TRPV5. The transcription of the target gene downstream of TRPV5 was detected by RT-PCR. NHX1 expression was significantly decreased in podocytes and high glucose-stimulated podocytes of diabetic nephropathy patients (P<0.05). After silencing NHX1, podocyte marker protein podocin expression was significantly decreased and podocyte activity was increased. The nuclear translocation of TRPV5 increased, and the transcription of the target gene downstream of TRPV5 increased (P < 0.05). In contrast, the expression of overexpressed NHX1 group was significantly increased, the activity of podocytes was decreased, the nuclear access of TRPV5 was decreased, and the transcription of the target gene downstream of TRPV5 was decreased (P<0.05). NHX1 may reduce podocyte injury in diabetic nephropathy by inhibiting TRPV5 entry into the nucleus.
VL  - 6
IS  - 5
ER  -

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