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CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model

Title
CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model
Authors
Uddin, Md JamalJeong, JeewonPak, Eun SeonHa, Hunjoo
Ewha Authors
하헌주Md Jamal Uddin
SCOPUS Author ID
하헌주scopus; Md Jamal Uddinscopus
Issue Date
2021
Journal Title
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
ISSN
1942-0900JCR Link

1942-0994JCR Link
Citation
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY vol. 2021
Publisher
HINDAWI LTD
Indexed
SCIE; SCOPUS WOS
Document Type
Article
Abstract
Acute kidney injury (AKI) most commonly appears in critically ill patients in hospitals. AKI is characterized as a quick deterioration of kidney function and has recently been identified to be tightly interlinked with chronic kidney diseases. The emerging major mediators of AKI include oxidative stress and endoplasmic reticulum (ER) stress. Carbon monoxide (CO) attenuates oxidative stress and ER stress in various cells, while Fyn, a member of the Src kinase family, is activated by oxidative stress and contributes to ER stress in skeletal muscle. Considering these, the objective of the current research was to determine (i) the involvement of Fyn in ER stress-mediated AKI and (ii) the effect of CO-releasing molecule-2 (CORM2) on reactive oxygen species- (ROS-) Fyn-ER stress-mediated AKI. Pretreatment with CORM2 (30 mg/kg) efficiently inhibited LPS (30 mg/kg)-induced oxidative stress, inflammation, and cellular apoptosis during AKI in C57BL/6J mice. Also, CORM2 efficiently suppressed the activation of Fyn and ER stress in AKI mice. Consistently, pretreatment with CORM2 inhibited oxidative stress, Fyn activation, ER stress, inflammation, and apoptosis in LPS- or H2O2-stimulated proximal epithelial tubular cells. Fyn inhibition using siRNA or an inhibitor (PP2) significantly attenuated ER stress responses in the cells. These data suggest that CORM2 may become a potential treatment option against ROS-Fyn-ER stress-mediated AKI.
DOI
10.1155/2021/9947772
Appears in Collections:
약학대학 > 약학과 > Journal papers
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