Isolation, Culture and Characterization of Human Renal Proximal Tubule and Collecting Duct Cells

1999 ◽  
Vol 7 (5-6) ◽  
pp. 353-359 ◽  
Author(s):  
Anna L. Trifillis
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Renal Proximal Tubule ◽  
Duct Cells ◽  
Collecting Duct Cells

scholarly journals Exosomal transfer from human renal proximal tubule cells to distal tubule and collecting duct cells

2014 ◽  
Vol 47 (15) ◽  
pp. 89-94 ◽  
Author(s):  
John J. Gildea ◽  
Joscelyn E. Seaton ◽  
Ken G. Victor ◽  
Camellia M. Reyes ◽  
Dora Bigler Wang ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Renal Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells

Alterations in cell-adhesive and migratory properties of proximal tubule and collecting duct cells from bcl-2 −/− mice

2004 ◽  
Vol 287 (6) ◽  
pp. F1154-F1163 ◽  
Author(s):  
Jacqueline Ziehr ◽  
Nader Sheibani ◽  
Christine M. Sorenson
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Proximal Tubule Cells ◽  
Duct Cells ◽  
Scratch Wound ◽  
Cell Adhesive ◽  
Scratch Wound Assay ◽  
Collecting Duct Cells ◽  
Tubule Cells ◽  
Sb 203580

Bcl-2 protects cells from apoptosis initiated by a variety of stimuli including loss of cell adhesion. Bcl-2 −/− mice develop renal hypoplastic/cystic dysplasia with renal cyst formation coinciding with renal maturation in normal mice. To gain a better understanding of the role cell-adhesive mechanisms play during renal maturation, we generated proximal tubule and collecting duct cell lines from postnatal day 10 ( P10) and P20 bcl-2 +/+ and bcl-2 −/− mice. Very little is known about the role cell-adhesive and migratory mechanisms play during renal maturation. We observed that modulation of cell-adhesive properties, which normally occur in a nephron segment-specific manner during renal maturation, and cell migration were altered in cells from bcl-2 −/− mice. Enhanced migration of bcl-2 −/− proximal tubule cells in a scratch wound assay was completely inhibited by incubation with PP1 (Src inhibitor) and moderately affected by incubation with SB-203580 (p38 inhibitor). These cells expressed increased levels of fibronectin and had numerous central focal adhesions. P20 bcl-2 −/− proximal tubule cells adhered to fibronectin but adhered poorly to collagen, vitronectin, or laminin. Collecting duct cells, similar to proximal tubule cells from bcl-2 −/− mice, demonstrated enhanced migration in a scratch wound assay that was inhibited by incubation with PP1. Migration of these cells was moderately affected by incubation with PD-98059 (MEK inhibitor) or LY-294002 (PI3 kinase inhibitor), whereas incubation with SB-203580 had no effect. P10 bcl-2 −/− collecting duct cells also expressed increased levels of fibronectin but decreased levels of thrombospondin-1 and demonstrated precocious binding to fibronectin and vitronectin compared with bcl-2 +/+ cells. The ability of P20 bcl-2 +/+ collecting duct cells to adhere to fibronectin and vitronectin corresponded with a decline in thrombospondin-1 expression. Therefore, alterations in cell-adhesive and migratory characteristics may be an early indicator of aberrant renal epithelial cell differentiation.

N-domain angiotensin-I converting enzyme is expressed in immortalized mesangial, proximal tubule and collecting duct cells

2015 ◽  
Vol 72 ◽  
pp. 380-390 ◽  
Author(s):  
Pamella Huey Mei Wang ◽  
Maria Claudina Andrade ◽  
Beata Marie Redublo Quinto ◽  
Giovana Di Marco ◽  
Renato Arruda Mortara ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme ◽  
Duct Cells ◽  
Collecting Duct Cells

scholarly journals Gender-Dependent Phenotype in Polycystic Kidney Disease Is Determined by Differential Intracellular Ca2+ Signals

2021 ◽  
Vol 22 (11) ◽  
pp. 6019
Author(s):  
Khaoula Talbi ◽  
Inês Cabrita ◽  
Rainer Schreiber ◽  
Karl Kunzelmann
Keyword(s):  
Cell Proliferation ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Collecting Duct ◽  
Primary Cells ◽  
Loss Of Function ◽  
Polycystic Kidney ◽  
Chloride Currents ◽  
Duct Cells ◽  
Collecting Duct Cells

Autosomal dominant polycystic kidney disease (ADPKD) is caused by loss of function of PKD1 (polycystin 1) or PKD2 (polycystin 2). The Ca2+-activated Cl− channel TMEM16A has a central role in ADPKD. Expression and function of TMEM16A is upregulated in ADPKD which causes enhanced intracellular Ca2+ signaling, cell proliferation, and ion secretion. We analyzed kidneys from Pkd1 knockout mice and found a more pronounced phenotype in males compared to females, despite similar levels of expression for renal tubular TMEM16A. Cell proliferation, which is known to be enhanced with loss of Pkd1−/−, was larger in male when compared to female Pkd1−/− cells. This was paralleled by higher basal intracellular Ca2+ concentrations in primary renal epithelial cells isolated from Pkd1−/− males. The results suggest enhanced intracellular Ca2+ levels contributing to augmented cell proliferation and cyst development in male kidneys. Enhanced resting Ca2+ also caused larger basal chloride currents in male primary cells, as detected in patch clamp recordings. Incubation of mouse primary cells, mCCDcl1 collecting duct cells or M1 collecting duct cells with dihydrotestosterone (DHT) enhanced basal Ca2+ levels and increased basal and ATP-stimulated TMEM16A chloride currents. Taken together, the more severe cystic phenotype in males is likely to be caused by enhanced cell proliferation, possibly due to enhanced basal and ATP-induced intracellular Ca2+ levels, leading to enhanced TMEM16A currents. Augmented Ca2+ signaling is possibly due to enhanced expression of Ca2+ transporting/regulating proteins.

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