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Role of GABA Receptors in Fetal Lung Development in Rats
Fluid accumulation is critical for lung distension and normal development. The multi-subunit γ-amino butyric acid type A receptors (GABA(A)) mainly act by mediating chloride ion (Cl(−)) fluxes. Since fetal lung actively secretes Cl(−)-rich fluid, we investigated the role of GABA(A) receptors in feta...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Public Library of Science
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994757/ https://www.ncbi.nlm.nih.gov/pubmed/21152393 http://dx.doi.org/10.1371/journal.pone.0014171 |
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author | Chintagari, Narendranath Reddy Jin, Nili Gao, Li Wang, Yang Xi, Dong Liu, Lin |
author_facet | Chintagari, Narendranath Reddy Jin, Nili Gao, Li Wang, Yang Xi, Dong Liu, Lin |
author_sort | Chintagari, Narendranath Reddy |
collection | PubMed |
description | Fluid accumulation is critical for lung distension and normal development. The multi-subunit γ-amino butyric acid type A receptors (GABA(A)) mainly act by mediating chloride ion (Cl(−)) fluxes. Since fetal lung actively secretes Cl(−)-rich fluid, we investigated the role of GABA(A) receptors in fetal lung development. The physiological ligand, GABA, and its synthesizing enzyme, glutamic acid decarboxylase, were predominantly localized to saccular epithelium. To examine the effect of activating GABA(A) receptors in fetal lung development in vivo, timed-pregnant rats of day 18 gestation underwent an in utero surgery for the administration of GABA(A) receptor modulators into the fetuses. The fetal lungs were isolated on day 21 of gestation and analyzed for changes in fetal lung development. Fetuses injected with GABA had a significantly higher body weight and lung weight when compared to phosphate-buffered saline (control)-injected fetuses. GABA-injected fetal lungs had a higher number of saccules than the control. GABA increased the number of alveolar epithelial type II cells as indicated by surfactant protein C-positive cells. However, GABA decreased the number of α-smooth muscle actin-positive myofibroblasts, but did not affect the number of Clara cells or alveolar type I cells. GABA-mediated effects were blocked by the GABA(A) receptor antagonist, bicuculline. GABA also increased cell proliferation and Cl(−) efflux in fetal distal lung epithelial cells. In conclusion, our results indicate that GABA(A) receptors accelerate fetal lung development, likely through an enhanced cell proliferation and/or fluid secretion. |
format | Text |
id | pubmed-2994757 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-29947572010-12-08 Role of GABA Receptors in Fetal Lung Development in Rats Chintagari, Narendranath Reddy Jin, Nili Gao, Li Wang, Yang Xi, Dong Liu, Lin PLoS One Research Article Fluid accumulation is critical for lung distension and normal development. The multi-subunit γ-amino butyric acid type A receptors (GABA(A)) mainly act by mediating chloride ion (Cl(−)) fluxes. Since fetal lung actively secretes Cl(−)-rich fluid, we investigated the role of GABA(A) receptors in fetal lung development. The physiological ligand, GABA, and its synthesizing enzyme, glutamic acid decarboxylase, were predominantly localized to saccular epithelium. To examine the effect of activating GABA(A) receptors in fetal lung development in vivo, timed-pregnant rats of day 18 gestation underwent an in utero surgery for the administration of GABA(A) receptor modulators into the fetuses. The fetal lungs were isolated on day 21 of gestation and analyzed for changes in fetal lung development. Fetuses injected with GABA had a significantly higher body weight and lung weight when compared to phosphate-buffered saline (control)-injected fetuses. GABA-injected fetal lungs had a higher number of saccules than the control. GABA increased the number of alveolar epithelial type II cells as indicated by surfactant protein C-positive cells. However, GABA decreased the number of α-smooth muscle actin-positive myofibroblasts, but did not affect the number of Clara cells or alveolar type I cells. GABA-mediated effects were blocked by the GABA(A) receptor antagonist, bicuculline. GABA also increased cell proliferation and Cl(−) efflux in fetal distal lung epithelial cells. In conclusion, our results indicate that GABA(A) receptors accelerate fetal lung development, likely through an enhanced cell proliferation and/or fluid secretion. Public Library of Science 2010-11-30 /pmc/articles/PMC2994757/ /pubmed/21152393 http://dx.doi.org/10.1371/journal.pone.0014171 Text en Chintagari et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Chintagari, Narendranath Reddy Jin, Nili Gao, Li Wang, Yang Xi, Dong Liu, Lin Role of GABA Receptors in Fetal Lung Development in Rats |
title | Role of GABA Receptors in Fetal Lung Development in Rats |
title_full | Role of GABA Receptors in Fetal Lung Development in Rats |
title_fullStr | Role of GABA Receptors in Fetal Lung Development in Rats |
title_full_unstemmed | Role of GABA Receptors in Fetal Lung Development in Rats |
title_short | Role of GABA Receptors in Fetal Lung Development in Rats |
title_sort | role of gaba receptors in fetal lung development in rats |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994757/ https://www.ncbi.nlm.nih.gov/pubmed/21152393 http://dx.doi.org/10.1371/journal.pone.0014171 |
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