cAMP regulation of Cl− and HCO 3 − secretion across rat fetal distal lung epithelial cells

Author:

Lazrak Ahmed1,Thome Ulrich2,Myles Carpantanto1,Ware Janice2,Chen Lan1,Venglarik Charles J.3,Matalon Sadis1234

Affiliation:

1. Departments of Anesthesiology,

2. Pediatrics,

3. Environmental Health Sciences, and

4. Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35233

Abstract

We isolated and cultured fetal distal lung epithelial (FDLE) cells from 17- to 19-day rat fetuses and assayed for anion secretion in Ussing chambers. With symmetrical Ringer solutions, basal short-circuit currents ( I sc) and transepithelial resistances were 7.9 ± 0.5 μA/cm2 and 1,018 ± 73 Ω · cm2, respectively (means ± SE; n = 12). Apical amiloride (10 μM) inhibited basal I sc by ∼50%. Subsequent addition of forskolin (10 μM) increased I sc from 3.9 ± 0.63 μA/cm2 to 7.51 ± 0.2 μA/cm2( n = 12). Basolateral bumetanide (100 μM) decreased forskolin-stimulated I sc from 7.51 ± 0.2 μA/cm2 to 5.62 ± 0.53, whereas basolateral 4,4′-dinitrostilbene-2,2′-disulfonate (5 mM), an inhibitor of HCO[Formula: see text] secretion, blocked the remaining I sc. Forskolin addition evoked currents of similar fractional magnitudes in symmetrical Cl- or HCO[Formula: see text]-free solutions; however, no response was seen using HCO[Formula: see text]- and Cl-free solutions. The forskolin-stimulated I sc was inhibited by glibenclamide but not apical DIDS. Glibenclamide also blocked forskolin-induced I sc across monolayers having nystatin-permeablized basolateral membranes. Immunolocalization studies were consistent with the expression of cystic fibrosis transmembrane conductance regulator (CFTR) protein in FDLE cells. In aggregate, these findings indicate the presence of cAMP-activated Cl and HCO[Formula: see text] secretion across rat FDLE cells mediated via CFTR.

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

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