Difference between revisions of "Dabrowska 2023 Int J Mol Sci"

Latest revision as of 14:34, 13 March 2024

Dabrowska A, Zajac M, Bednarczyk P, Lukasiak A (2023) Effect of quercetin on mitoBK_Ca channel and mitochondrial function in human bronchial epithelial cells exposed to particulate matter. Int J Mol Sci 24:638. https://doi.org/10.3390/ijms24010638

» PMID: 36614079 Open Access

Dabrowska Adrianna, Zajac Miroslaw, Bednarczyk Piotr, Lukasiak Agnieszka (2023) Int J Mol Sci

Abstract: Particulate matter (PM) exposure increases reactive oxygen species (ROS) levels. It can lead to inflammatory responses and damage of the mitochondria thus inducing cell death. Recently, it has been shown that potassium channels (mitoK) located in the inner mitochondrial membrane are involved in cytoprotection, and one of the mechanisms involves ROS. To verify the cytoprotective role of mitoBK_Ca, we performed a series of experiments using a patch-clamp, transepithelial electrical resistance assessment (TEER), mitochondrial respiration measurements, fluorescence methods for the ROS level and mitochondrial membrane potential assessment, and cell viability measurements. In the human bronchial epithelial cell model (16HBE14σ), PM < 4 μm in diameter (SRM-PM4.0) was used. We observed that PM decreased TEER of HBE cell monolayers. The effect was partially abolished by quercetin, a mitoBK_Ca opener. Consequently, quercetin decreased the mitochondrial membrane potential and increased mitochondrial respiration. The reduction of PM-induced ROS level occurs both on cellular and mitochondrial level. Additionally, quercetin restores HBE cell viability after PM administration. The incubation of cells with PM substantially reduced the mitochondrial function. Isorhamnetin had no effect on TEER, the mitoBK_Ca activity, respiratory rate, or mitochondrial membrane potential. Obtained results indicate that PM has an adverse effect on HBE cells at the cellular and mitochondrial level. Quercetin is able to limit the deleterious effect of PM on barrier function of airway epithelial cells. We show that the effect in HBE cells involves mitoBK_Ca channel-activation. However, quercetin’s mechanism of action is not exclusively determined by modulation of the channel activity. • Keywords: Epithelium, mitoBKCa channel, Mitochondria, Particulate matter, Quercetin • Bioblast editor: Plangger M • O2k-Network Lab: PL Warsaw Bednarczyk P

Labels: MiParea: Respiration, mt-Membrane, Pharmacology;toxicology

Stress:Oxidative stress;RONS Organism: Human Tissue;cell: Lung;gill, Endothelial;epithelial;mesothelial cell Preparation: Permeabilized cells, Intact cells

Regulation: Ion;substrate transport, mt-Membrane potential Coupling state: LEAK, ROUTINE, OXPHOS, ET Pathway: S, ROX HRR: Oxygraph-2k, O2k-Fluorometer

2024-03

@@ Line 1: / Line 1: @@
 {{Publication
-|title=Dabrowska A, Zajac M, Bednarczyk P, Lukasiak A (2023) Effect of Quercetin on mito<sub>BKCa</sub> channel and mitochondrial function in human bronchial epithelial cells exposed to particulate matter. Int J Mol Sci 24:638. https://doi.org/10.3390/ijms24010638
+|title=Dabrowska A, Zajac M, Bednarczyk P, Lukasiak A (2023) Effect of quercetin on mitoBK<sub>Ca</sub> channel and mitochondrial function in human bronchial epithelial cells exposed to particulate matter. Int J Mol Sci 24:638. https://doi.org/10.3390/ijms24010638
 |info=[https://pubmed.ncbi.nlm.nih.gov/36614079 PMID: 36614079 Open Access]
 |authors=Dabrowska Adrianna, Zajac Miroslaw, Bednarczyk Piotr, Lukasiak Agnieszka
 |year=2023
 |journal=Int J Mol Sci
-|abstract=Particulate matter (PM) exposure increases reactive oxygen species (ROS) levels. It can lead to inflammatory responses and damage of the mitochondria thus inducing cell death. Recently, it has been shown that potassium channels (mitoK) located in the inner mitochondrial membrane are involved in cytoprotection, and one of the mechanisms involves ROS. To verify the cytoprotective role of mito<sub>BKCa</sub>, we performed a series of experiments using a patch-clamp, transepithelial electrical resistance assessment (TEER), mitochondrial respiration measurements, fluorescence methods for the ROS level and mitochondrial membrane potential assessment, and cell viability measurements. In the human bronchial epithelial cell model (16HBE14σ), PM < 4 μm in diameter (SRM-PM4.0) was used. We observed that PM decreased TEER of HBE cell monolayers. The effect was partially abolished by quercetin, a mito<sub>BKCa</sub> opener. Consequently, quercetin decreased the mitochondrial membrane potential and increased mitochondrial respiration. The reduction of PM-induced ROS level occurs both on cellular and mitochondrial level. Additionally, quercetin restores HBE cell viability after PM administration. The incubation of cells with PM substantially reduced the mitochondrial function. Isorhamnetin had no effect on TEER, the mito<sub>BKCa</sub> activity, respiratory rate, or mitochondrial membrane potential. Obtained results indicate that PM has an adverse effect on HBE cells at the cellular and mitochondrial level. Quercetin is able to limit the deleterious effect of PM on barrier function of airway epithelial cells. We show that the effect in HBE cells involves mitomito<sub>BKCa</sub> channel-activation. However, quercetin’s mechanism of action is not exclusively determined by modulation of the channel activity.
+|abstract=Particulate matter (PM) exposure increases reactive oxygen species (ROS) levels. It can lead to inflammatory responses and damage of the mitochondria thus inducing cell death. Recently, it has been shown that potassium channels (mitoK) located in the inner mitochondrial membrane are involved in cytoprotection, and one of the mechanisms involves ROS. To verify the cytoprotective role of mitoBK<sub>Ca</sub>, we performed a series of experiments using a patch-clamp, transepithelial electrical resistance assessment (TEER), mitochondrial respiration measurements, fluorescence methods for the ROS level and mitochondrial membrane potential assessment, and cell viability measurements. In the human bronchial epithelial cell model (16HBE14σ), PM < 4 μm in diameter (SRM-PM4.0) was used. We observed that PM decreased TEER of HBE cell monolayers. The effect was partially abolished by quercetin, a mitoBK<sub>Ca</sub> opener. Consequently, quercetin decreased the mitochondrial membrane potential and increased mitochondrial respiration. The reduction of PM-induced ROS level occurs both on cellular and mitochondrial level. Additionally, quercetin restores HBE cell viability after PM administration. The incubation of cells with PM substantially reduced the mitochondrial function. Isorhamnetin had no effect on TEER, the mitoBK<sub>Ca</sub> activity, respiratory rate, or mitochondrial membrane potential. Obtained results indicate that PM has an adverse effect on HBE cells at the cellular and mitochondrial level. Quercetin is able to limit the deleterious effect of PM on barrier function of airway epithelial cells. We show that the effect in HBE cells involves mitoBK<sub>Ca</sub> channel-activation. However, quercetin’s mechanism of action is not exclusively determined by modulation of the channel activity.
 |keywords=Epithelium, mitoBKCa channel, Mitochondria, Particulate matter, Quercetin
 |editor=[[Plangger M]]
@@ Line 11: / Line 11: @@
 }}
 {{Labeling
-|area=Respiration
+|area=Respiration, mt-Membrane, Pharmacology;toxicology
-|instruments=Oxygraph-2k
+|injuries=Oxidative stress;RONS
+|organism=Human
+|tissues=Lung;gill, Endothelial;epithelial;mesothelial cell
+|preparations=Permeabilized cells, Intact cells
+|topics=Ion;substrate transport, mt-Membrane potential
+|couplingstates=LEAK, ROUTINE, OXPHOS, ET
+|pathways=S, ROX
+|instruments=Oxygraph-2k, O2k-Fluorometer
 |additional=2024-03
 }}