scholarly journals Characterization of Insulin-Like Growth Factor I Receptors on Madin-Darby Canine Kidney (MDCK) Cell Line

1987 ◽  
Vol 34 (3) ◽  
pp. 339-346 ◽  
Author(s):  
IZUMI SUKEGAWA ◽  
NAOMI HIZUKA ◽  
KAZUE TAKANO ◽  
KUMIKO ASAKAWA ◽  
KAZUO SHIZUME
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Mdck Cell ◽  
Insulin Like Growth Factor ◽  
Madin Darby Canine Kidney ◽  
Mdck Cell Line ◽  
Factor I ◽  
Darby Canine Kidney ◽  
Canine Kidney

scholarly journals Development of cell surface polarity in the epithelial Madin-Darby canine kidney (MDCK) cell line.

1984 ◽  
Vol 3 (11) ◽  
pp. 2687-2694 ◽  
Author(s):  
J. Balcarova-Ständer ◽  
S.E. Pfeiffer ◽  
S.D. Fuller ◽  
K. Simons
Keyword(s):  
Cell Surface ◽  
Cell Line ◽  
Mdck Cell ◽  
Surface Polarity ◽  
Madin Darby Canine Kidney ◽  
Mdck Cell Line ◽  
Darby Canine Kidney ◽  
Canine Kidney

Effects of hyperosmolarity on the Na+-myo-inositol cotransporter SMIT2 stably transfected in the Madin-Darby canine kidney cell line

2008 ◽  
Vol 295 (3) ◽  
pp. C791-C799 ◽  
Author(s):  
Pierre Bissonnette ◽  
Karim Lahjouji ◽  
Michael J. Coady ◽  
Jean-Yves Lapointe
Keyword(s):  
Cell Line ◽  
Mdck Cell ◽  
Time Course ◽  
Nuclear Translocation ◽  
Transport Systems ◽  
Madin Darby Canine Kidney ◽  
Exogenous Dna ◽  
Mdck Cell Line ◽  
Darby Canine Kidney ◽  
Canine Kidney

Myo-inositol (MI) is a compatible osmolyte used by cells to compensate for changes in the osmolarity of their surrounding milieu. In kidney, the basolateral Na+-MI cotransporter (SMIT1) and apical SMIT2 proteins are homologous cotransporters responsible for cellular uptake of MI. It has been shown in the Madin-Darby canine kidney (MDCK) cell line that SMIT1 expression was under the control of the tonicity-sensitive transcription factor, tonicity-responsive enhancer binding protein (TonEBP). We used an MDCK cell line stably transfected with SMIT2 to determine whether variations in external osmolarity could also affect SMIT2 function. Hyperosmotic conditions (+200 mosM raffinose or NaCl but not urea) generated an increase in SMIT2-specific MI uptake by three- to ninefold in a process that required protein synthesis. Using quantitative RT-PCR, we have determined that hyperosmotic conditions augment both the endogenous SMIT1 and the transfected SMIT2 mRNAs. Transport activities for both SMIT1 and SMIT2 exhibited differences in their respective induction profiles for both their sensitivities to raffinose, as well as in their time course of induction. Application of MG-132, which inhibits nuclear translocation of TonEBP, showed that the effect of osmolarity on transfected SMIT2 was unrelated to TonEBP, unlike the effect observed with SMIT1. Inhibition studies involving the hyperosmolarity-related MAPK suggested that p38 and JNK play a role in the induction of SMIT2. Further studies have shown that hyperosmolarity also upregulates another transfected transporter (Na+-glucose), as well as several endogenously expressed transport systems. This study shows that hyperosmolarity can stimulate transport in a TonEBP-independent manner by increasing the amount of mRNA derived from an exogenous DNA segment.

scholarly journals Characterization of Insulin-Like Growth Factor I Receptors on Human Erythroleukemia Cell Line (K-562 Cells)

1987 ◽  
Vol 34 (1) ◽  
pp. 81-88 ◽  
Author(s):  
NAOMI HIZUKA ◽  
IZUMI SUKEGAWA ◽  
KAZUE TAKANO ◽  
KUMIKO ASAKAWA ◽  
REIKO HORIKAWA ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Erythroleukemia Cell ◽  
Growth Factor I ◽  
K 562 Cells

Presence of a novel influx pathway for Mg2+ in MDCK cells

1990 ◽  
Vol 259 (3) ◽  
pp. C521-C525 ◽  
Author(s):  
G. A. Quamme ◽  
L. J. Dai
Keyword(s):  
Cell Line ◽  
Mdck Cell ◽  
Mdck Cells ◽  
Cell Types ◽  
Madin Darby Canine Kidney ◽  
Entry Pathway ◽  
Electrical Gradient ◽  
Free Media ◽  
Darby Canine Kidney ◽  
Canine Kidney

Basal free Mg2+ concentration was 0.49 +/- 0.03 mM in normal single Madin-Darby canine kidney (MDCK) cells as measured by fluorescence with the aid of mag-fura-2. Accordingly, Mg2+ may enter the cell down a transmembrane electrical gradient. The present study describes some aspects of Mg2+ entry into the established MDCK cell line. MDCK cells were Mg2(+)-depleted (0.26 +/- 0.01 mM) by culturing in Mg2(+)-free media for 16-20 h. Cells were subsequently exposed to 5 mM MgCl2, and intracellular Mg2+ concentration ([Mg2+]i) was monitored with fluorescence. [Mg2+]i returned to normal basal levels, 0.56 +/- 0.05 mM, with a refill rate of 272 +/- 39 nM/s, n = 4. Mg2+ entry was not changed by 5.0 mM external Ca2+ but was completely inhibited with 5.0 mM La3+. Intracellular Ca2+ concentration was not altered by Mg2+ depletion or during Mg2+ repletion. Mg2+ uptake was inhibited by verapamil (0 +/- 27 nM/s, n = 3), was inhibited less so by diltiazem (141 +/- 34 nM/s, n = 3), and was not affected by nifedipine (300 +/- 53 nM/s, n = 6). These inhibitors were fully reversible on removal, and [Mg2+]i returned to normal levels. These data indicate the presence of a unique Mg2+ entry pathway in MDCK cells that may be important in Mg2+ homeostasis. The model of Mg2+ refill into Mg2(+)-depleted cells may be useful in other cell types.

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