Postnatal disappearance of type A intercalated cells in carbonic anhydrase II-deficient mice

L. P. Brion, C. Suarez, P. Saenger

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Despite chronic acidosis, collecting ducts in adult carbonic anhydrase II-deficient (CAD mice) are depleted of intercalated cells, including those of type A, which are acid-secreting cells. We hypothesized that this depletion could occur during postnatal development. Principal cells were identified by immunofluorescence using an antibody to rat aquaporin-2 (AQP-2), and type A intercalated cells using an antibody specific for anion exchanger (AE1). In CAD mice the proportion of AQP2-positive cells, normal at 11 days, increased progressively in the cortical (CCD) and outer medullary collecting duct (OMCD), to reach almost 100% in the OMCD in adults. The percentage of AE1-positive cells in the OMCD of CAD mice decreased by half by 6 weeks of age and further by adulthood. In controls, however, the proportion of AQP2-positive cells and that of AE1-positive cells in the OMCD remained stable after 10 days of age. AE1-positive cells accounted for the majority of intercalated cells in the OMCD. The mechanisms leading to selective postnatal cell depletion in the collecting duct in CAD mice remain to be determined.

Original languageEnglish (US)
Pages (from-to)477-481
Number of pages5
JournalPediatric Nephrology
Volume16
Issue number6
DOIs
StatePublished - 2001

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Carbonic Anhydrase II
Aquaporin 2
Erythrocyte Anion Exchange Protein 1
Antibodies
Acidosis
Fluorescent Antibody Technique

Keywords

  • Anion-exchanger 1
  • Aquaporin-2
  • Carbonic anhydrase II-deficient
  • Immunohistochemistry
  • Intercalated cell
  • Mouse

ASJC Scopus subject areas

  • Nephrology
  • Pediatrics, Perinatology, and Child Health

Cite this

Postnatal disappearance of type A intercalated cells in carbonic anhydrase II-deficient mice. / Brion, L. P.; Suarez, C.; Saenger, P.

In: Pediatric Nephrology, Vol. 16, No. 6, 2001, p. 477-481.

Research output: Contribution to journalArticle

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