Ontogeny of Cell Type-Specific Enzyme Reactivities in Kidney Collecting Ducts

Holthöfer, Harry

doi:10.1203/00006450-198711000-00005

Cited by 28 publications

(14 citation statements)

References 13 publications

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“…1C). This greatly extends previous observations made at a single developmental time point in rabbit and human kidneys (13,14). At each developmental stage, apical membrane distribution of Na+/K+-ATPase was frequently found in the most immature collecting tubules of the outer cortical zone of active nephrogenesis, and it was only rarely demonstrated in the more mature collecting tubules of the medulla (Fig.…”

Section: Discussionsupporting

confidence: 72%

“…Alternatively, if Na+/K+-ATPase is mislocated to apical membranes of cystic tubular cells it could stimulate net basal-to-apical vectorial transport of Na+ and fluid, resulting in tubular fluid secretion and cyst formation (6,9). In this latter regard, it is of particular interest that Na+/K+-ATPase has been reported to be transiently expressed in the apical membrane of collecting tubule epithelium during normal renal development (13,14), and it is sorted to both apical and basal-lateral domains during establishment of polarity in MDCK cells, a canine renal epithelial cell line (15). Furthermore, Na+/K+-ATPase is normally expressed in the apical membrane of choroid plexus epithelia (16) and retinal pigmented epithelial cells (17).…”

mentioning

confidence: 99%

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Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease.

Avner

Sweeney

Nelson

1992

Proc. Natl. Acad. Sci. U.S.A.

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Congenital polycystic kidney disease is characterized by the formation of large fluid-filled cysts in kidney tubules. It has been postulated that increased epithelial cell proliferation and altered transtubular fluid transport are necessary for cyst formation. To address the latter problem, we have studied the plasma membrane distribution of the al and (31 subunits of Na+/K+-ATPase during progressive stages of proximal and collecting tubular cyst formation in the CPK mouse, a murine model of autosomal recessive polycystic kidney disease. In both control and cystic proximal tubules, Na+/K+-ATPase distribution was restricted to the basallateral membrane of cells. However, in newborn through day 5 kidney tissue, 16% of control vs. 47% of cystic outer cortical, 6% of control vs. 46% of cystic inner cortical, and 2% of control vs. 63% of cystic medullary collecting tubules demonstrated apical and lateral membrane distribution of Na+/K+-ATPase. In all nephrogenic zones, the percentage of control or cystic collecting tubules demonstrating apical membrane distribution of Na+/K+-ATPase decreased over time, but the percentage of cystic collecting tubules with apical membrane

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Section: Discussionsupporting

confidence: 72%

mentioning

confidence: 99%

Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease.

Avner

Sweeney

Nelson

1992

Proc. Natl. Acad. Sci. U.S.A.

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“…In mice, ICs are first observed in the developing medullary CD and connecting tubule, yet are not seen in the cortical CD throughout prenatal development. 20,21 In the immediate postnatal period, the IC distribution shifts from the inner medullary CD to the cortical CD, similar to the adult distribution across several species. 14,[22][23][24][25] The full extent of the effects of obstruction on CD epithelial remodeling and on postnatal CD physiology is unknown.…”

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confidence: 90%

Remodeling of the Fetal Collecting Duct Epithelium

Hiatt

Ivanova

Torán

et al. 2010

The American Journal of Pathology

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Congenital urinary tract obstruction induces changes to the renal collecting duct epithelium, including alteration and depletion of intercalated cells. To study the effects of obstruction on the ontogeny of intercalated cell development, we examined normal and obstructed human fetal and postnatal kidneys. In the normal human fetal kidney, intercalated cells originated in the medullary collecting duct at 8 weeks gestation and remained most abundant in the inner medulla throughout gestation. In the cortex, intercalated cells were rare at 18 and 26 weeks gestation and observed at low abundance at 36 weeks gestation. Although early intercalated cells exhibit an immature phenotype, Type A intercalated cells predominated in the inner and outer medullae at 26 and 36 weeks gestation with other intercalated cell subtypes observed rarely. Postnatally, the collecting duct epithelium underwent a remodeling whereby intercalated cells become abundant in the cortex yet absent from the inner medulla. In 18-week obstructed kidneys with mild to moderate injury, the intercalated cells became more abundant and differentiated than the equivalent age-matched normal kidney. In contrast, more severely injured ducts of the late obstructed kidney exhibited a significant reduction in intercalated cells. These studies characterize the normal ontogeny of human intercalated cell development and suggest that obstruction induces premature remodeling and differentiation of the fetal collecting duct epithelium.

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“…cell division) occurs between fetal life and postnatal d 15 (22), and functional maturation (i.e. differentiation) has been observed between postnatal d 12 and 30 (23,24).…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of Epidermal Growth Factor, Transforming Growth Factor-α, Epidermal Growth Factor Receptor, and Thyroid Hormone Receptor RNA Levels in Rat Kidney and Changes in Those Levels Induced by Early Thyroxine Treatment

et al. 1992

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ABSTRAm. Ontogenic changes in the mRNA levels of epidermal growth factor (EGF), transforming growth factor-a, EGF receptor, and thyroid hormone receptor (rerbA) were examined in developing rat kidneys. The mRNA levels of both EGF and thyroid hormone receptor rose dramatically during the postnatal period with the rise in thyroid hormone receptor message preceding the rise in EGF message. In addition, we examined renal mRNA levels in 1-wk-old rats treated with thyroxine (T4) from birth through d 6. Neonatal T4 treatment augmented the renal mRNA levels of EGF but decreased the levels of EGF-receptor and transforming growth factor-a. T4 treatment did not significantly affect the levels of renal mRNA for thyroid hormone receptor. Although the EGF and transforming growth factor-a peptides are similar and interact with the same receptor, our findings indicate that these homologous growth factors are regulated differently during development. In addition, hormones that influence growth and development, such as T4, may function both as positive and negative regulators of growth factor expression. (Pediatr Res 31: 330-334, 1992) born rodents (5, 6), and it has been proposed that EGF mediates these developmental effects of thyroid hormone (7).Thyroid hormones also have been shown to increase EGF as well as EGF mRNA levels in developing rodent kidneys (8). To more fully understand the interrelations among these polypeptide growth factors and thyroid hormones in developing rodent kidney, cDNA probes for EGF, TGF-a, EGF-R, and thyroid hormone receptor (r-erbA-P) were used to examine normal rat kidneys taken from animals ranging in age from 21 d postconception to adult. Northern blots were prepared and used to quantify changes in the relative amount of each message during development. The ontogenic changes in message levels were examined with respect to the normal postnatal increase in T4 secretion. In addition, newborn animals were injected with T4 for the first 6 d of life to prematurely increase circulating adult T4 levels. Northern blots prepared from the kidneys of treated and control animals were examined to determine the effect of T4 treatment on the message levels of EGF, TGF-a, EGF receptor, and thyroid hormone receptor. MATERIALS AND METHODS AbbreviationsSprague-Dawley rats were obtained from Simonson Laboratories. Date-bred rats from the same source provided the fetal EGF, epidermal growth factor and neonatal animals used in the study. The animals were TGF-a, transforming growth factor-a maintained in accordance with the NIH Guide for the Care and EGF-R, epidermal growth factor receptor Use of Laboratory Animals. For the T4 treatment studies, new-SSC, saline sodium citrate born rats were treated with T4 (0.4 yg/g body wt/d) from the day T3, triiodothronine of birth through d 6 of life; kidneys were collected on d 7. After T4, thyroxine decapitation, rat kidney tissues were removed, quickly frozen in poly A+, polyadenylated a bath of liquid nitrogen, and stored at -70°C. Before RNA extraction, the pooled kidney tissue...

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Ontogeny of Cell Type-Specific Enzyme Reactivities in Kidney Collecting Ducts

Cited by 28 publications

References 13 publications

Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease.

Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease.

Remodeling of the Fetal Collecting Duct Epithelium

Ontogeny of Epidermal Growth Factor, Transforming Growth Factor-α, Epidermal Growth Factor Receptor, and Thyroid Hormone Receptor RNA Levels in Rat Kidney and Changes in Those Levels Induced by Early Thyroxine Treatment

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