Naslov
Aquaporins and Nrf2: Partners in Regulating Cellular Oxidative Stress

Autori
Mlinarić, Monika ; Čipak Gašparović, Ana ; Abramov, Andrey Y.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
4th BenBedPhar Meeting - From Physiology to Pathology / - , 2023, 38-38

Skup
4th BenBedPhar Meeting - From Physiology to Pathology

Mjesto i datum
Zagreb, Hrvatska, 20.04.2023. - 21.04.2023

Vrsta sudjelovanja
Poster

Vrsta recenzije
Recenziran

Ključne riječi
AQP3 ; NRF2 ; oxidative stress

Sažetak
Aquaporins (AQPs) are membrane channels that facilitate the transport of water, glycerol, and other small solutes across the membrane in response to the osmotic gradient, and therefore play an important role in cell physiology. Peroxiporins, AQPs that transport hydrogen peroxide (H2O2), could play a role in the regulation of cellular oxidative status, consequently regulating important signaling pathways. Since they regulate H2O2 transport, there is a possible interaction between AQPs and Nrf2, the main regulator of antioxidant and cellular protective genes. We investigated AQP activity and their role in the regulation of oxidative stress by measuring the transport of H2O2 using fluorescent indicators Hyper-3 and OxiVision Green. Three non-selective AQP inhibitors (CuSO4, AgNO3, and NiCl2) were used to confirm the effect was due to AQPs, and Nrf2 was stimulated with Omaveloxolone to assess its potential effect on AQP activity. Cell death was evaluated with Hoechst and Propidium iodide staining, and reduced glutathione (GSH) levels in the cells were measured using the monochlorobimane (MCB) method to observe the effects of inhibiting AQP activity and stimulating Nrf2. Our results indicate that both inhibiting AQP activity and activating Nrf2 significantly reduced cell death. While treatment with AQP inhibitors showed some protective effect on GSH levels, Omaveloxolone was able to restore them to control levels. Furthermore, H2O2 influx to the cell was significantly reduced with both the inhibition of AQPs and activation of Nrf2, and the effect was amplified when both treatments were used together. These findings suggest that AQPs may play a critical role in regulating oxidative stress and that their activity may be modulated by Nrf2.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti

POVEZANOST RADA