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Inhibition of src family kinases ameliorates lps-induced acute kidney injury and mitochondrial dysfunction in mice

Title
Inhibition of src family kinases ameliorates lps-induced acute kidney injury and mitochondrial dysfunction in mice
Authors
Pak E.S.Uddin M.J.Ha H.
Ewha Authors
하헌주Md Jamal Uddin
SCOPUS Author ID
하헌주scopus
Issue Date
2020
Journal Title
International Journal of Molecular Sciences
ISSN
1661-6596JCR Link
Citation
International Journal of Molecular Sciences vol. 21, no. 21, pp. 1 - 17
Keywords
Acute kidney injuryInflammationMitochondrial biogenesisOxidative stressSrc family kinases inhibitor
Publisher
MDPI AG
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Acute kidney injury (AKI), a critical syndrome characterized by a rapid decrease of kidney function, is a global health problem. Src family kinases (SFK) are proto-oncogenes that regulate diverse biological functions including mitochondrial function. Since mitochondrial dysfunction plays an important role in the development of AKI, and since unbalanced SFK activity causes mitochondrial dysfunction, the present study examined the role of SFK in AKI. Lipopolysaccharides (LPS) inhibited mitochondrial biogenesis and upregulated the expression of NGAL, a marker of tubular epithelial cell injury, in mouse proximal tubular epithelial (mProx) cells. These alterations were prevented by PP2, a pan SFK inhibitor. Importantly, PP2 pretreatment significantly ameliorated LPS-induced loss of kidney function and injury including inflammation and oxidative stress. The attenuation of LPS-induced AKI by PP2 was accompanied by the maintenance of mitochondrial biogenesis. LPS upregulated SFK, especially Fyn and Src, in mouse kidney as well as in mProx cells. These data suggest that Fyn and Src kinases are involved in the pathogenesis of LPS-induced AKI, and that inhibition of Fyn and Src kinases may have a potential therapeutic effect, possibly via improving mitochondrial biogenesis. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
DOI
10.3390/ijms21218246
Appears in Collections:
약학대학 > 약학과 > Journal papers
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