scholarly journals Transcellular Transport of Vitamin B12in LLC-PK1 Renal Proximal Tubule Cells

2001 ◽  
Vol 12 (6) ◽  
pp. 1099-1106 ◽  
Author(s):  
RIKKE NIELSEN ◽  
BOE SANDAHL SØRENSEN ◽  
HENRIK BIRN ◽  
ERIK ILSØ CHRISTENSEN ◽  
EBBA NEXØ
Keyword(s):  
Proximal Tubule ◽  
Vitamin B ◽  
Proximal Tubule Cells ◽  
Transcellular Transport ◽  
Reverse Transcription Pcr ◽  
Affinity Ligand ◽  
Basolateral Side ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells ◽  
High Affinity Ligand

Abstract. The transcobalamin-vitamin B12complex is responsible for the transport of B12from plasma and into the tissues. The complex is filtered in the renal glomeruli and is a high-affinity ligand for the endocytic receptor megalin expressed in the proximal tubule. This study shows by the use of the proximal tubule LLC-PK1 cell line that transcobalamin-B12is internalized by megalin-mediated endocytosis. After endocytosis and accumulation in endosomes, transcobalamin is degraded and the B12molecule is released from the cells in complex with newly synthesized proteins. The release is polarized in such a way that vitamin in the apical medium is bound to proteins with the size of haptocorrin, whereas the B12released at the basolateral side is complexed to two different proteins with the sizes of transcobalamin and haptocorrin. Furthermore, transcobalamin mRNA was identified by reverse transcription-PCR in LLC-PK1 cells and human and pig kidney, whereas haptocorrin mRNA was identified only in LLC-PK1 cells. The results strongly suggest that megalin located in the proximal tubule cells is important for receptor-mediated tubular reabsorption followed by transcellular transport and release of vitamin B12complexed to newly synthesized carrier proteins. This mechanism is likely to play a significant role in the maintenance of B12homeostasis by returning filtered B12to the pool of circulating vitamin.

Effects of TCDD and estradiol-17β on the proliferation and Na+/glucose cotransporter in renal proximal tubule cells

2005 ◽  
Vol 19 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Ho Jae Han ◽  
Min Jin Lim ◽  
Yun Jung Lee ◽  
Eun Jung Kim ◽  
Young Jin Jeon ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells ◽  
Estradiol 17Β

Abstract P238: Regulation Of G Protein-coupled Receptor Kinase 4 Expression By Serum In Breast Cancer And Renal Proximal Tubule Cells

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Wei Yue ◽  
Peng Xu ◽  
John J Gildea ◽  
Robin A Felder
Keyword(s):  
Breast Cancer ◽  
Protein Synthesis ◽  
Proximal Tubule ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Renal Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells ◽  
G Protein Coupled

G protein-coupled receptor kinase 4 (GRK4) is a member of the GRK family which play critical role in regulation of the function of G protein-coupled receptors. Our previous studies have shown that GRK4 not only plays a role in regulating sodium excretion in renal proximal tubule cells but also acts as a stimulator on proliferation of breast cancer cells. Uncontrolled proliferation is a characteristics of cancer cells and GRK4 is upregulated in breast cancer cells. We hypothesized that expression of GRK4 may be regulated differently in cancer and non-cancer cells. To test this hypothesis, expression of GRK4 in response to serum was compared in breast cancer cells and renal proximal tubule cells by Western analysis. In three breast cancer cell lines serum withdrawal caused rapid reduction in the levels of GRK4 which occurred as early as 15 min. GRK4 levels correlated with the concentrations of serum added to the culture media. To determine if growth factors were a critical element for maintaining GRK4 levels in the cells, EGF (10-20 ng/ml) was added to serum free medium for 24 h. There was no increase in GRK4 levels in the cells treated with EGF compared with the serum starvation control. Similarly, serum withdrawal (16 h) led to 40-80% decrease of GRK4 levels in renal proximal tubule cells even in the presence of EFG supplement. Serum feeding for 30 min after starvation dramatically increased the levels of GRK4 in both breast cancer cells and RPTC which exceeded the steady state levels. This rapid recovery of GRK4 protein do not need de novo protein synthesis because pretreatment of the cells with protein synthesis inhibitor, cycloheximide (10 μg/ml, 24 h), did not prevent this event. Expression of GRK2, another member of the GRK family, was not affected by serum starvation. Our results have shown that GRK4 is very sensitive to serum concentration in breast cancer cells as well as in RPTC. Preliminary studies suggest that rapid protein degradation rather than shutting down the protein synthesis plays a major role in this kind of GRK4 regulation. The biological significance of serum regulation of GRK4 in cancer and non-cancerous cells needs further investigation.

Primary cultures of renal proximal tubule cells derived from individuals with primary hyperoxaluria

2009 ◽  
Vol 37 (3) ◽  
pp. 127-132 ◽  
Author(s):  
Karen L. Price ◽  
Sally-Anne Hulton ◽  
William G. van’t Hoff ◽  
John R. Masters ◽  
Gill Rumsby
Keyword(s):  
Proximal Tubule ◽  
Primary Cultures ◽  
Primary Hyperoxaluria ◽  
Renal Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells

scholarly journals Antenatal glucocorticoid treatment alters Na+ uptake in renal proximal tubule cells from adult offspring in a sex-specific manner

2015 ◽  
Vol 308 (11) ◽  
pp. F1268-F1275 ◽  
Author(s):  
Yixin Su ◽  
Jianli Bi ◽  
Victor M. Pulgar ◽  
Jorge Figueroa ◽  
Mark Chappell ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Fetal Programming ◽  
Specific Effect ◽  
Ang Ii ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells ◽  
Female Sheep ◽  
Male Sheep ◽  
In Cells

We have shown a sex-specific effect of fetal programming on Na+ excretion in adult sheep. The site of this effect in the kidney is unknown. Therefore, we tested the hypothesis that renal proximal tubule cells (RPTCs) from adult male sheep exposed to betamethasone (Beta) before birth have greater Na+ uptake than do RPTCs from vehicle-exposed male sheep and that RPTCs from female sheep similarly exposed are not influenced by antenatal Beta. In isolated RPTCs from 1- to 1.5-yr-old male and female sheep, we measured Na+ uptake under basal conditions and after stimulation with ANG II. To gain insight into the mechanisms involved, we also measured nitric oxide (NO) levels, ANG II receptor mRNA levels, and expression of Na+/H+ exchanger 3. Basal Na+ uptake increased more in cells from Beta-exposed male sheep than in cells from vehicle-exposed male sheep (400% vs. 300%, P < 0.00001). ANG II-stimulated Na+ uptake was also greater in cells from Beta-exposed males. Beta exposure did not increase Na+ uptake by RPTCs from female sheep. NO production was suppressed more by ANG II in RPTCs from Beta-exposed males than in RPTCs from either vehicle-exposed male or female sheep. Our data suggest that one site of the sex-specific effect of Beta-induced fetal programming in the kidney is the RPTC and that the enhanced Na+ uptake induced by antenatal Beta in male RPTCs may be related to the suppression of NO in these cells.

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