Next Article in Journal
Betacoronavirus Genomes: How Genomic Information has been Used to Deal with Past Outbreaks and the COVID-19 Pandemic
Previous Article in Journal
MicroRNAs as Key Players in Melanoma Cell Resistance to MAPK and Immune Checkpoint Inhibitors
Article

Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury

1
Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 7008558, Japan
2
Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 7008558, Japan
3
New Industry Creation Hatchery Center, Tohoku University, Sendai 9808575, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(12), 4545; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124545
Received: 19 May 2020 / Revised: 23 June 2020 / Accepted: 24 June 2020 / Published: 26 June 2020
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia–reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) and Vash2 homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration. View Full-Text
Keywords: acute kidney injury; ischemia-reperfusion; oxidative stress; vasohibin-2; peritubular capillaries acute kidney injury; ischemia-reperfusion; oxidative stress; vasohibin-2; peritubular capillaries
Show Figures

Figure 1

MDPI and ACS Style

Miyake, H.; Tanabe, K.; Tanimura, S.; Nakashima, Y.; Morioka, T.; Masuda, K.; Sugiyama, H.; Sato, Y.; Wada, J. Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury. Int. J. Mol. Sci. 2020, 21, 4545. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124545

AMA Style

Miyake H, Tanabe K, Tanimura S, Nakashima Y, Morioka T, Masuda K, Sugiyama H, Sato Y, Wada J. Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury. International Journal of Molecular Sciences. 2020; 21(12):4545. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124545

Chicago/Turabian Style

Miyake, Hiromasa, Katsuyuki Tanabe, Satoshi Tanimura, Yuri Nakashima, Tomoyo Morioka, Kana Masuda, Hitoshi Sugiyama, Yasufumi Sato, and Jun Wada. 2020. "Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury" International Journal of Molecular Sciences 21, no. 12: 4545. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124545

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop