In baby mouse kidney epithelial cells, paclitaxel was found to cause an increase in Bim protein levels that could be inhibited by H-ras expression.
Eileen White laboratory also found that the expression of Ras upregulated basal autophagy, which was required for immortal mouse kidney epithelial cells survival in starvation and in Ras-mediated tumorigenesis [ 52].
Figure 6 summarises the concentration ranges of CFTRinh-172 and GlyH-101 used by us and their corresponding effects on CFTR, VSORC and CaCC conductances, expressed in mouse kidney epithelial cells.
An examination of the frequency of mutations in mouse kidney epithelial cells at the same gene locus that had been examined in humans however revealed that mutation rates are roughly comparable [ 35].
White's group also found that Ras expression upregulates basal autophagy, which was required for survival of immortal mouse kidney epithelial cells during starvation and during Ras-mediated tumorigenesis [ 107].
This concept is supported by evidence that in mouse embryonic fibroblasts and in immortalized baby mouse kidney epithelial cells, overexpression of Bcl-2 (anti-apoptotic) or simultaneous knockdown of the pro-apoptotic Bcl-2-associated X protein (Bax) or Bcl-2-associated killer (Bak) and depletion of Beclin 1 (autophagic) lead to necrotic cell death when cells are exposed to hypoxia or etoposide.
For example, in the model of immortalised baby-mouse kidney epithelial cells, which undergo cell death in response to hypoxia by knockdown of the pro-apoptotic proteins (Bax and Bak), however, the overexpression of the antiapoptotic protein Bcl-2 causes a shift from apoptosis to autophagic cell death (Golstein and Kroemer, 2007).
First, to determine whether MEFs normally express PC1 at a level analogous to those of renal epithelial cells, we used quantitative real-time RT PCR to compare Pkd1 mRNA levels in Pkd1 +/+ and Pkd1 −/− MEFs with IMCD3 (inner medullary collecting duct) cells, which are frequently used to study PC1 function, and with mPKE (non-immortalized mouse primary kidney epithelial) cells.
In the present study, we tested whether treatment with polyphenols affected the content or biosynthesis of Q. Mouse kidney proximal tubule epithelial (Tkpts) cells and human embryonic kidney cells 293 (HEK 293) were treated with several types of polyphenols, and kaempferol produced the largest increase in Q levels.
mpkCCDc14 cells (mouse kidney distal tubule epithelial cells, a gift from Dr. E. Feraille, University of Geneva) were cultured in 1∶1 DmediumMF12 medium, supplemented with 5 µg/ml insulin, 50 nM dexamethasone, 60 nM selenium, 5 µg/ml transferrin, 1 nM triiodothyronine, 10 ng/ml epidermal growth factor (EGF), 20 mM HEPES, 2 mM glutamine, 10% fetal bovine serum (FBS) and 20 mM D-glucose.
Both studies used ATCC strain 19698 and different infection models (Balb/c mice and bovine kidney epithelial cells) [ 30, 31], and the consistency between these studies and our data suggests that these genes are very likely to be important for the survival of MAP in a mammalian host.
