Tubulocystic epithelium

Wilson, Patricia D.; Sherwood, Ann C.

doi:10.1038/ki.1991.56

Cited by 73 publications

(29 citation statements)

References 127 publications

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“…The current data demonstrate that intratubular cyst fluid accumulation in this nephron segment is not secondary to simple reversal of vectorial Na+ and fluid transport as has been proposed for ADPKD epithelium (6,9). Instead, proximal tubular cyst formation in this murine model of ARPKD may involve increased organic anion secretion driven by a basal-lateral membrane Na+/K+-ATPase (8,12,33 (19) in outer cortex (A), inner cortex (B), and medulla (C).…”

Section: Discussionmentioning

confidence: 87%

“…If present in its normal basallateral membrane location, increased Na+/K+-ATPase activity in cystic tubular epithelium might lead to increased secondary active transport and net tubular secretion of solutes, thereby osmotically obligating intratubular fluid accumulation (2,5,12). 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).…”

mentioning

confidence: 99%

“…Such studies, as well as mathematical analysis of cyst growth kinetics and meticulous anatomical study of ADPKD, demonstrate that two basic criteria necessary for cyst formation are increased epithelial cell proliferation and altered transtubular fluid transport (3)(4)(5)(6).…”

mentioning

confidence: 99%

“…Altered fluid transport in renal cystic tubular epithelium leading to net tubular secretion and intratubular fluid accumulation could result from alterations in ion pump activity or more global abnormalities of polarized cell structure and function (2,5,6). Studies in the C57BL/6Jcpk/cpk (CPK) mouse, a murine model of ARPKD (2,7,8), and cultured ADPKD cystic epithelium (6, 9) suggest a significant role for altered Na+/K+ adenosine triphosphatase (Na+/K+-ATPase) activity in cystic tubular epithelial fluid secretion.…”

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: Discussionmentioning

confidence: 87%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

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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“…Formation and expansion of "in vitro" cysts, derived from solitary human cortex cells, depends from the coordinated interplay among cellular proliferation, fluid secretion and remodeling of extracellular matrix surrounding cysts (8)(9). The molecular mechanism and the pathogenesis of cyst formation are still unclear.…”

Section: Discussionmentioning

confidence: 99%

Simple Renal Cysts in Hypertensive Patients: Relation between Cyst Growing and Anti-Hypertensive Therapy

Schiavone

Salvatore

Primavera

et al. 2003

Int J Immunopathol Pharmacol

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Focal adhesion kinase, paxillin, and Bcl-2: Analysis of expression, phosphorylation, and association during morphogenesis

Sorenson

Sheibani

1999

Dev. Dyn.

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Cell adhesive mechanisms which determine tissue architecture during morphogenesis are tightly regulated and have an impact on apoptosis, cell migration, proliferation, and differentiation. Bcl‐2 is a death repressor that protects cells from apoptosis initiated by a variety of stimuli including loss of cell adhesion. Utilizing the kidney as a model of an organ that undergoes three‐dimensional development we demonstrate that bcl‐2 directly associates with paxillin. Focal adhesion kinase (FAK)(p125) and paxillin(p68) were highly expressed and tyrosine phosphorylated during development but declined to low levels following renal maturation (postnatal day 20) in normal mice. The decline in the expression of p125 FAK and p68 paxillin occurred together with an increase in specific cleavage products of lower molecular weights. Mice deficient in bcl‐2 are born with renal hypoplasia and succumb to renal failure as a result of renal multicystic disease. In kidneys from postnatal day 20 bcl‐2 −/− mice, tyrosine phosphorylation of p125 FAK and p68 paxillin was not down‐regulated. However, the level of expression was similar to that of normal mice. These results demonstrate that the developmentally regulated expression and phosphorylation of FAK and paxillin, in the presence of bcl‐2, is necessary for normal morphogenesis. The interaction of paxillin with bcl‐2 during nephrogenesis may provide an alternative to integrin(s) signaling through paxillin/FAK thus bypassing the need for adhesion‐mediated survival during three dimensional morphogenesis. Dev Dyn 1999;215:371–382. © 1999 Wiley‐Liss, Inc.

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Tubulocystic epithelium

Cited by 73 publications

References 127 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.

Simple Renal Cysts in Hypertensive Patients: Relation between Cyst Growing and Anti-Hypertensive Therapy

Focal adhesion kinase, paxillin, and Bcl-2: Analysis of expression, phosphorylation, and association during morphogenesis

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