Research output: Contribution to journal › Article › peer-review
Short Term Exposure of Sheep Tracheal Epithelium to Cigarette Smoke Extract Reduces ENaC Current: A Pilot Study. / Jagirdar, Rajesh M.; Grammatikopoulos, Alexandros; Ioannou, Maria et al.
In: In Vivo, Vol. 38, No. 5, 01.09.2024, p. 2294-2299.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - Short Term Exposure of Sheep Tracheal Epithelium to Cigarette Smoke Extract Reduces ENaC Current: A Pilot Study
AU - Jagirdar, Rajesh M.
AU - Grammatikopoulos, Alexandros
AU - Ioannou, Maria
AU - Solenov, Evgeniy
AU - Gourgoulianis, Konstantinos I.
AU - Hatzoglou, Chrissi
AU - Giannou, Anastasios D.
AU - Mercanoglou, Baris
AU - Zarogiannis, Sotirios G.
PY - 2024/9/1
Y1 - 2024/9/1
N2 - Background/Aim: Cigarette smoke has been shown to induce a phenotype in humans known as “acquired cystic fibrosis”. This occurs because the cystic fibrosis transmembrane conductance regulator (CFTR) functions are impaired systemically due to the deleterious effects of smoke components. Elucidation of cigarette smoke effects on the tracheal epithelium is important. The aim of this study was to develop an ex vivo sheep tracheal model to investigate tracheal ion function. In this model, the epithelial sodium channel (ENaC) is inhibited after exposure to cigarette smoke extract (CSE) as a proof of principle. Materials and Methods: Tracheas were isolated from healthy sheep and the tracheal epithelium was surgically excised. Tissues were mounted in Ussing chambers and the short circuit current (Isc) was measured after incubation with 5% CSE in PBS or PBS alone for 30 min. The function of ENaC was investigated by the addition of amiloride (10–5M) apically. Western blot analysis was performed to assess differences in ENaC quantity after CSE exposure. Some specimens were stained with H&E for detection of histological alterations. Results: The amiloride effect on normal epithelium led to a significant decrease in Isc [ΔI=33±5.92 μA/cm2; p
AB - Background/Aim: Cigarette smoke has been shown to induce a phenotype in humans known as “acquired cystic fibrosis”. This occurs because the cystic fibrosis transmembrane conductance regulator (CFTR) functions are impaired systemically due to the deleterious effects of smoke components. Elucidation of cigarette smoke effects on the tracheal epithelium is important. The aim of this study was to develop an ex vivo sheep tracheal model to investigate tracheal ion function. In this model, the epithelial sodium channel (ENaC) is inhibited after exposure to cigarette smoke extract (CSE) as a proof of principle. Materials and Methods: Tracheas were isolated from healthy sheep and the tracheal epithelium was surgically excised. Tissues were mounted in Ussing chambers and the short circuit current (Isc) was measured after incubation with 5% CSE in PBS or PBS alone for 30 min. The function of ENaC was investigated by the addition of amiloride (10–5M) apically. Western blot analysis was performed to assess differences in ENaC quantity after CSE exposure. Some specimens were stained with H&E for detection of histological alterations. Results: The amiloride effect on normal epithelium led to a significant decrease in Isc [ΔI=33±5.92 μA/cm2; p
KW - Amiloride
KW - Ussing system
KW - cigarette smoke extract
KW - electrophysiology
KW - epithelial sodium channel
KW - tracheal epithelium
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85202569690&origin=inward&txGid=b568dfb28271b1d6f7da0b8a73fb8138
UR - https://www.mendeley.com/catalogue/4bdbf07e-fa82-3da5-b642-6245763f0f9f/
U2 - 10.21873/invivo.13694
DO - 10.21873/invivo.13694
M3 - Article
C2 - 39187341
VL - 38
SP - 2294
EP - 2299
JO - In Vivo
JF - In Vivo
SN - 1791-7549
IS - 5
ER -
ID: 60836319