Literature DB >> 9843757

Developmental regulation of epithelial sodium channel subunit mRNA expression in rat colon and lung.

S Watanabe1, K Matsushita, J B Stokes, P B McCray.   

Abstract

Na+ absorption via amiloride-sensitive Na+ channels is of critical importance in the transition between fetal and neonatal life in several tissues, including the colon, lung, and kidney. To characterize and contrast the mRNA expression of each of the three epithelial Na+ channel complex (ENaC) subunits, we conducted RNase protection assays (RPA) and in situ hybridization in colon and lung in fetal (17, 19, 20, and 21 days) and postnatal (1, 3, 9, 15, and 30 days) rats (r). In the colon the alpha-, beta-, and gamma-rENaC subunits showed quantitatively different but qualitatively similar expression. All three subunits gradually increased in abundance from fetal day 19 through day 30 of life. The amount of each subunit on day 30 was approximately three times the amount at day 1. In situ hybridization showed that each subunit was localized to the surface epithelial cells with minimal expression in the crypts. The lung showed a completely different pattern. In contrast to the colon, the total amount of alpha-rENaC mRNA (by RPA) in the lung increased dramatically from fetal day 19 to 21, whereas beta- and gamma-rENaC showed modest prenatal increases. The amounts of all three mRNAs fell after birth through day 9 (to about 75% of the day 1 value). On days 15 and 30 the amount of mRNA rose to approach the values on day 1. alpha-rENaC mRNA abundance always exceeded beta- and gamma-rENaC, and the quantitative expression was different for alpha- than for beta- and gamma-rENaC. In situ hybridization studies showed that all three subunits were expressed in epithelial cells of the bronchi, bronchioles, and alveoli and not in blood vessels. These studies show striking developmental heterogeneity in rENaC mRNA expression between lung and colon, probably reflecting different developmental regulatory mechanisms in these organs.

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Year:  1998        PMID: 9843757     DOI: 10.1152/ajpgi.1998.275.6.G1227

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  5 in total

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Journal:  Proc Natl Acad Sci U S A       Date:  2002-02-12       Impact factor: 11.205

Review 2.  ENaCs and ASICs as therapeutic targets.

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Journal:  Infect Immun       Date:  1999-09       Impact factor: 3.441

4.  NKCC-1 and ENaC are down-regulated in nitrofen-induced hypoplastic lungs with congenital diaphragmatic hernia.

Authors:  Andreas Ringman; Marina Zelenina; Ann-Christine Eklöf; Anita Aperia; Björn Frenckner
Journal:  Pediatr Surg Int       Date:  2008-07-31       Impact factor: 1.827

5.  Expression of ENaC subunits, chloride channels, and aquaporins in ovine fetal lung: ontogeny of expression and effects of altered fetal cortisol concentrations.

Authors:  Nathan M Jesse; Jarret McCartney; Xiaodi Feng; Elaine M Richards; Charles E Wood; Maureen Keller-Wood
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2009-06-10       Impact factor: 3.619

  5 in total

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