Basic ResearchIL-17C has a pathogenic role in kidney ischemia/reperfusion injury
Graphical abstract
Section snippets
Renal IL-17C was increased in human beings with AKI
To explore changes of renal IL-17C in AKI, IL-17C was measured by real-time quantitative polymerase chain reaction and immunohistochemistry. In a group of patients with AKI, renal IL-17C mRNA levels were increased significantly compared with control subjects (P < 0.05), as shown in Figure 1a. Furthermore, renal TNF-α and IL-1β were increased remarkably, consistent with IL-17C (Figure 1b and c). Consistently, renal IL-17C protein was expressed principally in renal tubular epithelial cells, and
Discussion
Inflammation has been identified as a key driving force in the pathophysiology of AKI. Renal tubular epithelial cells are extremely vulnerable to intrinsic oxidative stress because of their structure and function, particularly during the reperfusion phase of IRI.25 Necrotic cells release damage-associated molecules, which can activate resident kidney cells and immune effector cells, thus triggering an immune response.26 Proinflammatory and anti-inflammatory mediators released by activated
Human kidney biopsy samples
The use of human medical information and kidney samples was approved by the Ethics Committee of Shanghai Jiao Tong University Affiliated Sixth People’s Hospital. This research was performed in accordance with the World Medical Association Declaration of Helsinki, and all subjects provided written informed consent. Subjects diagnosed with AKI and control subjects diagnosed with no obvious kidney pathology were enrolled and clinical data were recorded as described previously.42 AKI was diagnosed
Disclosure
All the authors declared no competing interests.
Acknowledgments
This work was supported by grants from the National Natural Science Foundation of China (81770741).
Author Contributions
FW designed and led the study; FW and YL drafted the manuscript; YL, JY, XL, GZ, YK, ZL, and RW performed the experiments; FW, FZ, NW, and TX performed data analysis; and TX and YQ provided reagents and technical support.
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2021, Experimental Cell ResearchCitation Excerpt :The activation of the ADB2 signal in macrophages can induce the expression of TIM3, promote the change of anti-inflammatory phenotype of macrophages, block systemic inflammation caused by lipopolysaccharide, and protect the kidney from IRI [7]. Wang Feng et al. have reported that inhibiting IL-17C or blocking IL-17RE may be a new strategy for the treatment of AKI induced by IRI [8]. In addition, the level of endogenous ATIII also plays a key role in regulating the development of AKI; ATIII is a serine protease inhibitor and glycoprotein synthesized in the liver and circulated in the blood, which has a strong anti-inflammatory effect; clinically, it is observed that patients with low activity of ATIII have a higher risk of AKI after cardiac surgery [9].
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FW and JY are co-first authors.