Developmental changes in carbonic anhydrase II in the rat kidney

Karashima, Shinnyo; Hattori, Shinzaburo; Ushijima, Tadashi; Furuse, Akio; Nakazato, Hitoshi; Matsuda, Ichiro

doi:10.1007/s004670050450

Cited by 26 publications

(6 citation statements)

References 24 publications

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“…NBC-1 activity at the basolateral membrane is also decreased in neonatal rabbits, but this activity is relatively more mature than the NHE-3 activity at the apical membrane [53]. Maturation of CA II and CA IV activities may also play an important role, since these enzymes are insufficiently expressed during the first 2 weeks of life in rat and rabbit kidneys, respectively [54,55]. The maturational increase of proximal tubular reabsorption of HCO 3 takes place pari passu with parallel increases in proximal tubular basolateral surface area and Na + , K + -ATPase activity [56,57,58].…”

Section: Ontogeny Of Renal Acidificationmentioning

confidence: 99%

New insights into the pathogenesis of renal tubular acidosis - from functional to molecular studies

Rodríguez‐Soriano¹

2000

Pediatric Nephrology

115

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The diagnosis and classification of renal tubular acidosis (RTA) have traditionally been made on the basis of functional studies. On these grounds, RTA has been separated into three main categories: (1) proximal RTA, or type 2; (2) distal RTA, or type 1; and (3) hyperkalemic RTA, or type 4. In recent years significant advances have been made in our understanding of the subcellular mechanisms involved in renal bicarbonate (HCO3-) and H+ transport. Application of molecular biology techniques has also opened a completely new perspective to the understanding of the pathophysiology of inherited cases of RTA. Mutations in the gene SLC4A4, encoding Na+-HCO3- cotransporter (NBC-1), have been found in proximal RTA with ocular abnormalities; in the gene SLC4A1, encoding Cl(-)-HCO3- exchanger (AE1), in autosomal dominant distal RTA; in the gene ATP6B1, encoding B1 subunit of H+-ATPase, in autosomal recessive distal RTA with sensorineural deafness; and in the gene CA2, encoding carbonic anhydrase II, in autosomal recessive osteopetrosis. Syndromes of aldosterone resistance have been also characterized molecularly and mutations in the gene MLR, encoding mineralocorticoid receptor, and in the genes SNCC1A, SNCC1B, and SCNN1G, encoding subunits of the epithelial Na+ channel, have been found in dominant and recessive forms of pseudohypoaldosteronism type 1, respectively. It can be concluded that, although functional studies are still necessary, a new molecular era in the understanding of disorders of renal acidification has arrived.

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Section: Ontogeny Of Renal Acidificationmentioning

confidence: 99%

New insights into the pathogenesis of renal tubular acidosis - from functional to molecular studies

Rodríguez‐Soriano¹

2000

Pediatric Nephrology

115

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“…Immaturity of these transporters results in decreased activity of the sodium‐ potassium transport system in the neonatal rodent and human (Evan et al, ; Ingulli and Mak, ). In rats, carbonic anhydrase II levels increase from 14% to 40% of adult levels from PND 7 to 21 (Karashima et al, ). Renal phosphate transport in rats also reaches maturity by PND 21, corresponding to the time of weaning.…”

Section: Postnatal Nephrotoxicitymentioning

confidence: 99%

Species Differences in Renal Development and Associated Developmental Nephrotoxicity

Frazier

2017

Birth Defects Research

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The developing kidney is sensitive to both morphological and functional disturbances during the gestational and postnatal phases of growth and differentiation. Exposure to drugs or chemicals during these critical windows of renal development can result in aplasia, dysplasia, polycystic kidney disease, hydronephrosis, or other features characteristic of nephrotoxicity, including tubule dilation, necrosis, or mineralization. Functional effects can occur without associated morphological abnormalities. Differences in the timing of nephrogenesis and morphologic renal development among species help to explain specific phenotypes of various gestational and postnatal teratogens and nephrotoxins. Functional maturation follows anatomical maturation, but important differences in maximally achieved glomerular filtration rate, concentrating ability and acid-base equilibrium between species makes comparison of these timings critical for accurate and consistent translation of laboratory animal toxicity data to the human clinical experience. Species and age dependent differences in the maturation of kidney transporters, renal xenobiotic metabolism and renal blood flow can have a profound effect on the toxicity profiles of agents and marked differences in the tolerability based on age. Advances in the understanding of the genetics of inherited renal diseases and the underlying cellular and molecular pathogenesis of renal developmental anomalies has helped provide mechanistic understanding of many teratogenic and perinatal nephrotoxic agents. Investigative studies have provided important translational and mechanistic information for assessing human pediatric nephrotoxic potential. Birth Defects Research 109:1243-1256, 2017. © 2017 Wiley Periodicals, Inc.

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“…After birth, carbonic anhydrase IV abundance and activity increase as a prerequisite for urinary acidification in both the proximal tubule and medullary collecting duct [39,50]. Similarly, in rats, carbonic anhydrase II in the initial segment of the proximal tubule and in the CCD and OMCD increases in parallel during the first weeks of life [19].…”

Section: Introductionmentioning

confidence: 96%

Postnatal expression of transport proteins involved in acid?base transport in mouse kidney

Bonnici

Wagner

2004

Pfl�gers Archiv European Journal of Physiology

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The kidney plays a major role in maintaining and controlling systemic acid-base homeostasis by reabsorbing bicarbonate and secreting protons and acidequivalents, respectively. During postnatal kidney development and adaptation to changing diets, plasma bicarbonate levels are increasing, the capacity for urinary acidification maturates, and the final morphology and distribution of intercalated cells is achieved. In adult kidney, at least two types of intercalated cells (IC) are found along the collecting duct characterised either by the expression of AE1 (type A IC) or pendrin (non-type A IC) where non-type A IC are found only in the convoluted distal tubule, connecting tubule and cortical collecting duct. Here we investigated in mouse kidney the relative mRNA abundance, protein expression levels and distribution of several proteins involved in renal acid-base transport, namely, the Na + /HCO 3 − cotransporter NBC1 (SLC4A4), the Na + /H + -exchanger NHE3 (SLC9A3), two subunits of the vacuolar H + -ATPase [ATP6V0A4 (a4), ATP6V1B1 (B1)], the Cl − /HCO 3 − exchangers AE1 (SLC4A1) and pendrin (SLC26A4). Relative mRNA abundance of all transport proteins was lowest at day 3 after birth and increased thereafter in parallel with protein levels. The numbers of type A and non-type A IC in the cortical collecting duct (CCD) increased from day 3 to days 18 and 24, whereas the number of IC in the CCD with apical staining for the vacuolar H + -ATPase subunits a4 and B1 decreased from day 3 to days 18 and 24, respectively. In addition, cells with characteristics of nontype A IC (pendrin expression, basolateral expression of vacuolar H + -ATPase subunits) were found in the inner and outer medulla 3 days after birth but were absent from the medulla of 24-day-old mice. Taken together, these results demonstrate massive changes in mRNA and protein expression levels of several acid-base transporters during postnatal kidney maturation and also show changes in intercalated cell phenotype in the medulla during these processes.

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Developmental changes in carbonic anhydrase II in the rat kidney

Cited by 26 publications

References 24 publications

New insights into the pathogenesis of renal tubular acidosis - from functional to molecular studies

New insights into the pathogenesis of renal tubular acidosis - from functional to molecular studies

Species Differences in Renal Development and Associated Developmental Nephrotoxicity

Postnatal expression of transport proteins involved in acid?base transport in mouse kidney

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