β2-Agonist regulation of cell volume in fetal distal lung epithelium by CAMP-independent Ca2+ release from intracellular stores

1997 ◽  
Vol 75 (8) ◽  
pp. 1030-1033 ◽  
Author(s):  
N Niisato ◽  
T Nakahari ◽  
A K Tanswell ◽  
Y Marunaka
Keyword(s):  
Cell Volume ◽  
Lung Epithelium ◽  
Distal Lung ◽  
Β2 Agonist

Effect of Covalent Serpin–Heparinoid Complexes on Plasma Thrombin Generation on Fetal Distal Lung Epithelium

2003 ◽  
Vol 28 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Leslie R. Berry ◽  
Petr Klement ◽  
Maureen Andrew ◽  
Anthony K. C. Chan
Keyword(s):  
Thrombin Generation ◽  
Lung Epithelium ◽  
Distal Lung

GATA6 regulates differentiation of distal lung epithelium

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2233-2246 ◽  
Author(s):  
Honghua Yang ◽  
Min Min Lu ◽  
Lili Zhang ◽  
Jeffrey A. Whitsett ◽  
Edward E. Morrisey
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Surfactant Protein ◽  
Gata Factor ◽  
Lung Epithelium ◽  
Alveolar Epithelial ◽  
Distal Lung ◽  
Transgenic Embryos

GATA6 is a member of the GATA family of zinc-finger transcriptional regulators and is the only known GATA factor expressed in the distal epithelium of the lung during development. To define the role that GATA6 plays during lung epithelial cell development, we expressed a GATA6-Engrailed dominant-negative fusion protein in the distal lung epithelium of transgenic mice. Transgenic embryos lacked detectable alveolar epithelial type 1 cells in the distal airway epithelium. These embryos also exhibited increased Foxp2 gene expression, suggesting a disruption in late alveolar epithelial differentiation. Alveolar epithelial type 2 cells, which are progenitors of alveolar epithelial type 1 cells, were correctly specified as shown by normal thyroid transcription factor 1 and surfactant protein A gene expression. However, attenuated endogenous surfactant protein C expression indicated that alveolar epithelial type 2 cell differentiation was perturbed in transgenic embryos. The number of proximal airway tubules is also reduced in these embryos, suggesting a role for GATA6 in regulating distal-proximal airway development. Finally, a functional role for GATA factor function in alveolar epithelial type 1 cell gene regulation is supported by the ability of GATA6 to trans-activate the mouse aquaporin-5 promoter. Together, these data implicate GATA6 as an important regulator of distal epithelial cell differentiation and proximal airway development in the mouse.

Heparan sulfates expressed in the distal lung are required for Fgf10 binding to the epithelium and for airway branching

2003 ◽  
Vol 285 (4) ◽  
pp. L838-L846 ◽  
Author(s):  
Konstantin I. Izvolsky ◽  
Lin Zhong ◽  
Lin Wei ◽  
Qiang Yu ◽  
Matthew A. Nugent ◽  
...  
Keyword(s):  
Developmental Stages ◽  
Binding Assay ◽  
Sodium Chlorate ◽  
Lung Epithelium ◽  
Organ Cultures ◽  
Additional Mechanism ◽  
Lung Morphogenesis ◽  
Distal Lung ◽  
Heparan Sulfates ◽  
Airway Branching

Fibroblast growth factor (Fgf) 10 is a critical regulator of bud formation during lung morphogenesis. fgf10 is expressed in distal lung mesenchyme at sites of prospective budding from the earliest developmental stages and signals through its epithelial receptor Fgfr2b. Experiments in intact lung organ cultures demonstrate that Fgf10 is a chemotactic factor for distal, but not for proximal, epithelium. This differential response suggests the involvement of an additional mechanism regulating Fgf10-Fgfr2b interactions, because Fgfr2b is uniformly expressed throughout the respiratory tract. Here we use an immunohistochemistry-based binding assay to show that O-sulfated heparan sulfates (HS) are critical for Fgf10 binding to the distal epithelium. We show that altering endogenous gradients of HS sulfation with sodium chlorate or over- O-sulfated synthetic heparin in lung organ cultures dramatically decreases Fgf10 binding. Moreover, we show that under these conditions epithelial binding is not improved by providing exogenous FGF10. Our data suggest that, not only ligand availability, but also the presence of specific patterns of HS modification in the distal lung epithelium are critical determinants of Fgf10 binding to the epithelium and signaling.

Regulation of whole cell currents by cytosolic cAMP, Ca2+, and Cl- in rat fetal distal lung epithelium

1995 ◽  
Vol 269 (1) ◽  
pp. C156-C162 ◽  
Author(s):  
T. Nakahari ◽  
Y. Marunaka
Keyword(s):  
Lung Epithelium ◽  
Cellular Mechanisms ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Whole Cell ◽  
Whole Cell Patch Clamp ◽  
Lung Epithelial ◽  
Distal Lung ◽  
Adrenergic Receptor Agonist ◽  
K Currents

The whole cell patch-clamp technique was used to study ionic conductances in fetal distal lung epithelial (FDLE) cells. In unstimulated FDLE cells, K+ conductances were detected in lowered intracellular Cl- concentration ([Cl-]i, < or = 50 mM). The whole cell currents of FDLE cells were increased by elevation of intracellular Ca2+ concentration ([Ca2+]i) or intracellular adenosine 3',5'-cyclic monophosphate (cAMP) concentration ([cAMP]i). The elevation of [Ca2+]i activated the K+ currents. The amiloride-blockable whole cell currents were activated by [cAMP]i of 1 mM with [Cl-]i of 20 mM and were more frequently detected in the pipette solution without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) than with it (0.5 mM). When the [Cl-]i was fixed at 50 or 145 mM, however, the increase in these currents was not detected even with cAMP and without EGTA. The amiloride-blockable currents were detected in both the Na+ and K+ pipette solutions. Thus the increase in amiloride-blockable whole cell currents was due to the activation of nonselective cation channels. In FDLE cells treated with terbutaline, which is a beta 2-adrenergic receptor agonist, or forskolin, these currents were detected in the pipette solution containing 20 mM Cl- but were suppressed with time when the pipette solution contained 50 or 145 mM Cl-. It seems likely that maintenance of [Cl-]i at the lowered level is an important requirement for the FDLE cells to activate the amiloride-blockable whole cell currents. It is proposed that cellular mechanisms, such as cell shrinkage, exist to reduce the [Cl-]i in response to cAMP.

The Differentiation of Distal Lung Epithelium from Embryonic Stem Cells

2007 ◽  
Author(s):  
Benjamin E. Van Vranken ◽  
Helen J. Rippon ◽  
Ali Samadikuchaksaraei ◽  
Alan O. Trounson ◽  
Anne E. Bishop
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Lung Epithelium ◽  
Distal Lung

Invited Review: Clearance of lung liquid during the perinatal period

2002 ◽  
Vol 93 (4) ◽  
pp. 1542-1548 ◽  
Author(s):  
Pierre M. Barker ◽  
Richard E. Olver
Keyword(s):  
Developmental Regulation ◽  
Perinatal Period ◽  
Lung Epithelium ◽  
Physiological Mechanisms ◽  
Transgenic Cell ◽  
Membrane Transport Proteins ◽  
Liquid Absorption ◽  
Clinical Consequences ◽  
Distal Lung ◽  
Lung Liquid

At birth, the distal lung epithelium undergoes a profound phenotypic switch from secretion to absorption in the course of adaptation to air breathing. In this review, we describe the developmental regulation of key membrane transport proteins and the way in which epinephrine, oxygen, glucocorticoids, and thyroid hormones interact to bring about this crucial change in function. Evidence from molecular, transgenic, cell culture, and whole lung studies is presented, and the clinical consequences of the failure of the physiological mechanisms that underlie perinatal lung liquid absorption are discussed.

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

2002 ◽  
Vol 82 (3) ◽  
pp. 569-600 ◽  
Author(s):  
Michael A. Matthay ◽  
Hans G. Folkesson ◽  
Christine Clerici
Keyword(s):  
Pulmonary Edema ◽  
Fluid Transport ◽  
Convincing Evidence ◽  
Lung Epithelium ◽  
Molecular Transporters ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Pathological Conditions ◽  
Distal Airway ◽  
Distal Lung

The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

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