scholarly journals Differential control of murine aldose reductase and fibroblast growth factor (FGF)-regulated-1 gene expression in NIH 3T3 cells by FGF-1 treatment and hyperosmotic stress

1997 ◽  
Vol 328 (2) ◽  
pp. 593-598 ◽  
Author(s):  
Debbie K. W. HSU ◽  
Yan GUO ◽  
A. Kimberly PEIFLEY ◽  
A. Jeffrey WINKLES
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Aldose Reductase ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Quiescent Cells ◽  
Nih 3T3 ◽  
Stimulation Of

Aldose reductase (AR) is an NADPH-dependent aldo-keto reductase implicated in cellular osmoregulation and detoxification. Two distinct murine genes have been identified that are predicted to encode proteins with significant amino acid sequence identity with mouse AR: mouse vas deferens protein and fibroblast growth factor (FGF)-regulated-1 protein (FR-1). Here we report that the AR and FR-1 genes are differentially regulated in NIH 3T3 fibroblasts. FGF-1 stimulation of quiescent cells induces both AR and FR-1 mRNA levels, but the effect on FR-1 mRNA expression is significantly greater. FGF-1 treatment also increases FR-1 protein expression, as determined by Western-blot analysis using FR-1-specific polyclonal antiserum. Calf serum stimulation of quiescent cells increases AR mRNA expression but not FR-1 mRNA expression. Finally, when NIH 3T3 cells are grown in hypertonic medium, AR mRNA levels are significantly increased whereas FR-1 mRNA levels are only slightly up-regulated. These results indicate that the AR and FR-1 genes are differentially regulated in murine fibroblasts by two different growth-promoting agents and by hyperosmotic stress. Therefore these structurally related enzymes may have at least some distinct cellular functions; for example, although both AR and FR-1 activity may be important for the metabolic changes associated with cellular proliferation, AR may be the primary aldo-keto reductase involved in cellular osmoregulation.

scholarly journals Fibroblast growth factor-1 stimulation of quiescent NIH 3T3 cells increases G/T mismatch-binding protein expression

1996 ◽  
Vol 319 (1) ◽  
pp. 9-12 ◽  
Author(s):  
Patrick J. DONOHUE ◽  
Sheau-Line Y. FENG ◽  
Gregory F ALBERTS ◽  
Yan GUO ◽  
Kimberly A PEIFLEY ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Binding Protein ◽  
Calf Serum ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Polypeptide growth factors promote cell-cycle progression in part by the transcriptional activation of a diverse group of specific genes. We have used an mRNA differential-display approach to identify several fibroblast growth factor (FGF)-1 (acidic FGF)-inducible genes in NIH 3T3 cells. Here we report that one of these genes, called FGF-regulated (FR)-3, is predicted to encode G/T mismatch-binding protein (GTBP), a component of the mammalian DNA mismatch correction system. The murine GTBP gene is transiently expressed after FGF-1 or calf serum treatment, with maximal mRNA levels detected at 12 and 18 h post-stimulation. FGF-1-stimulated NIH 3T3 cells also express an increased amount of GTBP as determined by immunoblot analysis. These results indicate that elevated levels of GTBP may be required during the DNA synthesis phase of the cell cycle for efficient G/T mismatch recognition and repair.

Fibroblast Growth Factor-1 Induction of Delayed-Early mRNA Expression in NIH 3T3 Cells Is Prolonged by Heparin Addition

1997 ◽  
Vol 234 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Patrick J. Donohue ◽  
Debbie K.W. Hsu ◽  
Yan Guo ◽  
Wilson H. Burgess ◽  
Jeffrey A. Winkles
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Fibroblast growth factor 23 production in bone is directly regulated by 1α,25-dihydroxyvitamin D, but not PTH

2010 ◽  
Vol 299 (5) ◽  
pp. F1212-F1217 ◽  
Author(s):  
Fumie Saji ◽  
Takashi Shigematsu ◽  
Toshifumi Sakaguchi ◽  
Masaki Ohya ◽  
Hikari Orita ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Insufficiency ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
Dihydroxyvitamin D ◽  
Fgf23 Concentration ◽  
Group A

Fibroblast growth factor 23 (FGF23), which is primarily produced by osteocytes in bone, regulates renal phosphate excretion and 1α,25-dihydroxyvitamin D [1,25(OH)2D3] metabolism. Patients with chronic kidney disease (CKD) have increased levels of circulating serum FGF23, but the direct effect on circulating FGF23 levels in renal insufficiency is still unclear. To identify the major regulator of FGF23 synthesis in renal insufficiency, we compared the effect of parathyroid hormone (PTH) and 1,25(OH)2D3 on FGF23 synthesis in the calvariae of normal rats with that of uremic rats in vitro. 1,25(OH)2D3 treatment significantly increased the FGF23 concentration in the medium from both groups, but the degree of increase in the uremic group was markedly higher than in the control group. A significant increase in FGF23 mRNA expression occurred as early as 4 h after treatment and reached the maximum within 8 h in the uremic group, whereas in the normal group a significant increase in FGF23 mRNA expression was observed only at 8 h. In addition, the expression of vitamin D receptor (VDR) mRNA in the calvariae of uremic rats was markedly higher than in normal rats. However, in neither group did PTH treatment affect the medium FGF23 concentration or the FGF23 mRNA levels. These results suggest that FGF23 synthesis in bone is regulated by 1,25(OH)2D3 directly, not by PTH, and that increased VDR mRNA expression induced the relatively swift and strong response in the uremic group.

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