UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms

Chuanxiu Yang, Lijing Su, Yang Wang, Lin Liu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current (I sc) of AEC II but decreased Isc of AEC I. The Cl - channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc (ΔIsc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced ΔIsc in AEC I, but not in AEC II. The general blocker of K + channels, BaCl2, eliminated the UTP-induced ΔIsc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl- secretion in AEC II and Cl - absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl- flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.

Original languageEnglish (US)
Pages (from-to)L439-L454
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume297
Issue number3
DOIs
StatePublished - Sep 1 2009
Externally publishedYes

Fingerprint

Alveolar Epithelial Cells
Uridine Triphosphate
Ion Transport
Epithelial Sodium Channels
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Fluids and Secretions
Amiloride
Signal Transduction

Keywords

  • Fluid transport
  • Short-circuit current

ASJC Scopus subject areas

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

Cite this

UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms. / Yang, Chuanxiu; Su, Lijing; Wang, Yang; Liu, Lin.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 297, No. 3, 01.09.2009, p. L439-L454.

Research output: Contribution to journalArticle

@article{09eeb5fe3e0d47bda789f9a0f06eb484,
title = "UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms",
abstract = "UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current (I sc) of AEC II but decreased Isc of AEC I. The Cl - channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc (ΔIsc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced ΔIsc in AEC I, but not in AEC II. The general blocker of K + channels, BaCl2, eliminated the UTP-induced ΔIsc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl- secretion in AEC II and Cl - absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl- flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.",
keywords = "Fluid transport, Short-circuit current",
author = "Chuanxiu Yang and Lijing Su and Yang Wang and Lin Liu",
year = "2009",
month = "9",
day = "1",
doi = "10.1152/ajplung.90268.2008",
language = "English (US)",
volume = "297",
pages = "L439--L454",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms

AU - Yang, Chuanxiu

AU - Su, Lijing

AU - Wang, Yang

AU - Liu, Lin

PY - 2009/9/1

Y1 - 2009/9/1

N2 - UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current (I sc) of AEC II but decreased Isc of AEC I. The Cl - channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc (ΔIsc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced ΔIsc in AEC I, but not in AEC II. The general blocker of K + channels, BaCl2, eliminated the UTP-induced ΔIsc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl- secretion in AEC II and Cl - absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl- flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.

AB - UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current (I sc) of AEC II but decreased Isc of AEC I. The Cl - channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc (ΔIsc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced ΔIsc in AEC I, but not in AEC II. The general blocker of K + channels, BaCl2, eliminated the UTP-induced ΔIsc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl- secretion in AEC II and Cl - absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl- flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.

KW - Fluid transport

KW - Short-circuit current

UR - http://www.scopus.com/inward/record.url?scp=68949114321&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=68949114321&partnerID=8YFLogxK

U2 - 10.1152/ajplung.90268.2008

DO - 10.1152/ajplung.90268.2008

M3 - Article

C2 - 19542245

AN - SCOPUS:68949114321

VL - 297

SP - L439-L454

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 3

ER -