Nitric Oxide Plays a Dual Role in Cardiorenal Syndrome in Vitro Model.

Autor:	Armentano GM; Laboratory of Cardiovascular Immunology, Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, SP, Brazil, marcela.ramos@ufabc.edu.br., Pieretti JC; Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, SP, Brazil., Falconi CA; Laboratory of Cardiovascular Immunology, Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, SP, Brazil., Seabra AB; Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, SP, Brazil., Carneiro-Ramos MS; Laboratory of Cardiovascular Immunology, Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, SP, Brazil.
Jazyk:	angličtina
Zdroj:	Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology [Cell Physiol Biochem] 2024 Jan 22; Vol. 58 (1), pp. 33-48.
DOI:	10.33594/000000681
Abstrakt:	Background/aims: Nitric oxide (NO) plays a dual role, acting as both an oxidant and a reducer, with various effects depending on its concentration and environment. Acute kidney injury's (AKI) pathogenesis observed in cardiorenal syndrome 3 (CRS 3) involves inflammatory responses and the production of reactive oxygen and nitrogen species. However, the role of NO on the development of CRS 3 is still not completely understood. The study aimed to mimic CRS 3 in vitro and investigate NO signaling and inflammatory molecules. Methods: Thus, HEK293 cells were submitted to normoxia (NX) or hypoxia (HX) protocols for 16 h followed by 3 h of reoxygenation, treated or not with L-NAME. Conditionate medium by HEK293 was transferred to H9c2 for 24 h. Cellular viability was evaluated by MTT assay, real time PCR was used to analyze gene expression and NO content were evaluated in the intra and extracellular medium by amperimetry. Results: Carbonic anhydrase 9 (CA9) expression increased 2.9-fold after hypoxia. Hypoxia reduced 18 % cell viability in HEK293 that was restored by L-NAME treatment. The sum of nitrite (NO2-) and S-nitrosothiol (S-NO) fractions in HEK293 cells showed a substantial decrease on NO intracellular content (38 %). Both IL-6 and IL-10 decreased in all groups compared to NX cells. Besides TNF-α and Bax/Bcl2 ratio increased in hypoxia (approximately 120-fold and 600-fold, respectively) and L-NAME restored this effect. Regarding H9c2 cells, the S-NO fractions showed a substantial decrease in extracellular content after HX (17%) that was not restored by L-NAME. IL-1β decreases in cardiac cells treated with conditioned medium from HX/L-NAME. Conclusion: In conclusion this study highlights the complex interplay of NO and inflammatory factors in hypoxia-induced renal and cardiac cell responses, with potential implications for cardiorenal syndrome. Competing Interests: The authors have nothing to disclose. (© Copyright by the Author(s). Published by Cell Physiol Biochem Press.)
Databáze:	MEDLINE
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