Document Detail

Cell type-specific acquired protection from crystal adherence by renal tubule cells in culture.
MedLine Citation:
PMID:  10201007     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Adherence of crystals to the surface of renal tubule epithelial cells is considered an important step in the development of nephrolithiasis. Previously, we demonstrated that functional monolayers formed by the renal tubule cell line, Madin-Darby canine kidney (MDCK), acquire protection against the adherence of calcium oxalate monohydrate crystals. We now examined whether this property is cell type specific. The susceptibility of the cells to crystal binding was further studied under different culture conditions. METHODS: Cell-type specificity and the influence of the growth substrate was tested by comparing calcium oxalate monohydrate crystal binding to LLC-PK1 cells and to two MDCK strains cultured on either permeable or impermeable supports. These cell lines are representative for the renal proximal tubule (LLC-PK1) and distal tubule/collecting duct (MDCK) segments of the nephron, in which crystals are expected to be absent and present, respectively. RESULTS: Whereas relatively large amounts of crystals adhered to subconfluent MDCK cultures, the level of crystal binding to confluent monolayers was reduced for both MDCK strains. On permeable supports, MDCK cells not only obtained a higher level of morphological differentiation, but also acquired a higher degree of protection than on impermeable surfaces. Crystals avidly adhered to LLC-PK1 cells, irrespective of their developmental stage or growth substrate used. CONCLUSIONS: These results show that the prevention of crystal binding is cell type specific and expressed only by differentiated MDCK cells. The anti-adherence properties acquired by MDCK cells may mirror a specific functional characteristic of its in situ equivalent, the renal distal tubule/collecting ducts.
C F Verkoelen; B G van der Boom; D J Kok; A B Houtsmuller; P Visser; F H Schröder; J C Romijn
Related Documents :
20617137 - Expression of nestin, vimentin, and ncam by renal interstitial cells after ischemic tub...
15610237 - Myocilin is expressed in the glomerulus of the kidney and induced in mesangioproliferat...
8719877 - The hepatocyte growth factor/scatter factor (hgf/sf) receptor, met, transduces a morpho...
22209527 - Pp1-mediated moesin dephosphorylation couples polar relaxation to mitotic exit.
10986477 - Modulation of cell and dna damage by poly(adp)ribose polymerase in lung cells exposed t...
22783847 - Effect of modifying quantum dot surface charge on airway epithelial cell uptake in vitro.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Kidney international     Volume:  55     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  1999 Apr 
Date Detail:
Created Date:  1999-07-14     Completed Date:  1999-07-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1426-33     Citation Subset:  IM    
Department of Urology, Erasmus University, Rotterdam, The Netherlands.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Calcium Oxalate / metabolism
Cell Adhesion / physiology
Cell Line
Cell Size / physiology
Diffusion Chambers, Culture
Kidney Tubules, Collecting / cytology,  metabolism*,  ultrastructure
Kidney Tubules, Proximal / cytology,  metabolism*,  ultrastructure
LLC-PK1 Cells
Microscopy, Confocal
Microscopy, Electron, Scanning
Ouabain / metabolism
Sodium-Potassium-Exchanging ATPase / metabolism
Time Factors
Reg. No./Substance:
25454-23-3/Calcium Oxalate; 630-60-4/Ouabain; EC ATPase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Hypertonicity-induced accumulation of organic osmolytes in papillary interstitial cells.
Next Document:  Phosphate depletion in the rat: effect of bisphosphonates and the calcemic response to PTH.