scholarly journals Adipose cell differentiation: evidence for a two-step process in the polyamine-dependent Ob1754 clonal line

1986 ◽  
Vol 238 (1) ◽  
pp. 115-122 ◽  
Author(s):  
E Z Amri ◽  
C Dani ◽  
A Doglio ◽  
J Etienne ◽  
P Grimaldi ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Mrna Level ◽  
Growth Arrest ◽  
Clonal Line ◽  
Adipose Cell ◽  
Step Process ◽  
Late Emergence ◽  
Adipose Conversion ◽  
Early Expression ◽  
Glycerol 3 Phosphate Dehydrogenase

A subclone of preadipocyte Ob17 cells has been isolated (Ob1754 clonal line). Confluent Ob1754 cells treated with an inhibitor of spermidine and spermine synthesis, methylglyoxal bis(guanylhydrazone), were totally dependent upon putrescine addition for the expression of glycerol-3-phosphate dehydrogenase which behaved as a late marker of adipose conversion. Under these conditions, the early expression of lipoprotein lipase during growth arrest remained unchanged. Studies at the mRNA level showed that the expression of unidentified pOb24 and pGH3 mRNAs, which was parallel to that of lipoprotein lipase, is independent of polyamine addition whereas the late emergence of glycerol-3-phosphate dehydrogenase mRNA was putrescine-dependent and co-ordinated with the expression of pAL422 mRNA encoding for a myelin-P2 homologue [Bernlohr, Angus, Lane, Bolanowski & Kelly (1984) Proc. Natl. Acad. Sci. U.S.A. 81, 5468-5472]. The appearance of lipoprotein lipase preceded DNA synthesis and post-confluent mitoses which were both putrescine-dependent and which took place before the appearance of glycerol-3-phosphate dehydrogenase. Thus the adipose conversion of Ob1754 cells involves the expression of at least two separate sets of markers which are differently regulated.

scholarly journals Effects of photoperiod and feeding level on adipose tissue and muscle lipoprotein lipase activity and mRNA level in dry non-pregnant sheep

2001 ◽  
Vol 85 (3) ◽  
pp. 299-306 ◽  
Author(s):  
Y. Faulconnier ◽  
M. Bonnet ◽  
F. Bocquier ◽  
C. Leroux ◽  
Y. Chilliard
Keyword(s):  
Cardiac Muscle ◽  
Lipoprotein Lipase ◽  
Fatty Acid Synthase ◽  
Mrna Level ◽  
Energy Requirements ◽  
Mrna Levels ◽  
Feeding Level ◽  
Pregnant Sheep ◽  
Cardiac Muscles ◽  
Glycerol 3 Phosphate Dehydrogenase

The aim of the present study was to investigate the effects of photoperiod and feeding level on lipid metabolism in ovine perirenal and subcutaneous adipose tissues (AT) and in skeletal and cardiac muscles. Twenty dry non-pregnant ovariectomised ewes were divided into two groups and subjected to either 8 h or 16 h light/d, and underfed at 22 % energy requirements for 7 d. Half of the ewes in each group were slaughtered and the remaining ewes were refed at 190 % energy requirements for 14 d, until slaughtering. Refeeding increased (2.6–4.3-fold) malic enzyme (ME), fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH) and glycerol-3-phosphate dehydrogenase (G3PDH) activities in subcutaneous AT as well as lipoprotein lipase (LPL) activity in perirenal (3.5-fold) and subcutaneous (10-fold) AT and to a lesser extent (1.4-fold) in the skeletal longissimus thoracis and cardiac muscles. Moreover, variations of LPL mRNA level followed variations of LPL activity: refeeding increased perirenal AT- and cardiac muscle-mRNA levels (7.4- and 2-fold respectively). The main finding of this study is that, for a given level of food intake, long days (compared with short days) increased the LPL activity in the longissimus thoracis muscle and, in refed ewes, the activities of LPL and ME in subcutaneous AT. Furthermore, long days increased LPL mRNA level in cardiac muscle and perirenal AT. Thus, our results show that there are direct effects of photoperiod on sheep AT lipogenic potential, as well as on muscle LPL activity, which are not caused by changes in nutrient availability.

scholarly journals Role of spermidine in the expression of late markers of adipose conversion Effects of growth hormone

1986 ◽  
Vol 239 (2) ◽  
pp. 363-370 ◽  
Author(s):  
E Z Amri ◽  
R Barbaras ◽  
A Doglio ◽  
C Dani ◽  
P Grimaldi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Mrna Level ◽  
Fold Increase ◽  
Intracellular Concentration ◽  
Polyamine Content ◽  
Adipose Conversion ◽  
Highly Correlated ◽  
Glycerol 3 Phosphate Dehydrogenase

Confluent Ob1771 cells treated with an inhibitor of spermidine and spermine synthesis, methylglyoxyal bis(guanylhydrazone), were dependent on putrescine addition for the expression of glycerol-3-phosphate dehydrogenase and acyl-CoA synthetase, which behaved as late markers of adipose conversion. A similar dependence was observed with drug-treated Ob17MT18 and 3T3-F442A preadipocyte cells, but not with non-differentiating 3T3-C2 cells. Studies in drug-treated Ob1771 cells at the mRNA level showed that the parallel expression of mRNAs encoding for glycerol-3-phosphate dehydrogenase and an homologue of serine proteinases of Mr 28,000 [Cook, Groves, Min & Spiegelman (1985) Proc. Natl. Acad. Sci. U.S.A. 82, 6480-6484] was also dependent on putrescine addition. Double-isotope experiments with [14C]putrescine and [3H]spermidine, as well as analysis of the polyamine content in drug-treated Ob1771 cells under various conditions, demonstrate after putrescine addition that the expression of late markers of adipose conversion was highly correlated with a 2-fold increase in the intracellular concentration of spermidine. No correlation was observed with changes in the intracellular concentrations of putrescine and spermine. Long-term exposure of untreated Ob1771 cells to growth hormone, which led to the expression of late markers of adipose conversion [Doglio, Dani, Grimaldi & Ailhaud (1986) Biochem. J. 238, 123-129] was also accompanied by the same increase in spermidine concentration, which attained values identical with those determined in drug-treated cells supplemented with putrescine. This observation suggests that the permissive effect of growth hormone on the terminal differentiation of adipose cells might e related to changes in the intracellular concentration of spermidine.

scholarly journals Growth hormone regulation of the expression of differentiation-dependent genes in preadipocyte Ob1771 cells

1986 ◽  
Vol 238 (1) ◽  
pp. 123-129 ◽  
Author(s):  
A Doglio ◽  
C Dani ◽  
P Grimaldi ◽  
G Ailhaud
Keyword(s):  
Growth Hormone ◽  
Mrna Level ◽  
Protein A ◽  
Transcriptional Level ◽  
Hormone Regulation ◽  
Beta Actin ◽  
Adipose Conversion ◽  
Specific Mrnas ◽  
Actin Mrna ◽  
Glycerol 3 Phosphate Dehydrogenase

The adipose conversion of Ob1771 preadipocytes, during exposure to medium containing bovine serum and supplemented with growth hormone, is accompanied by the acquisition of phenotypic markers and the increased accumulation of specific mRNAs. The expression of lipoprotein lipase, and that of unidentified pOb24 and pGH3 mRNAs, are early events which are independent of growth hormone supplementation. By contrast, the late expression of mRNAs encoding for glycerol-3-phosphate dehydrogenase and p422 protein (a myelin-P2 homologue) and that of glycerol-3-phosphate dehydrogenase activity require the presence of growth hormone. The abundance of beta-actin mRNA does not change during differentiation. Runoff transcription by nuclei isolated from untreated or growth hormone-treated cells reveal little or no change in the rates of transcription of pOb24, pGH3 and beta-actin mRNAs. By contrast, the transcription rate of the p422 gene increases markedly (greater than 6-fold) in nuclei of growth hormone-treated cells. However, the p422 mRNA is more abundant than would be predicted by its nuclear transcription alone, suggesting, in Ob1771 cells exposed to growth hormone, that there is a post-transcriptional level of control. These results indicate that the permissive role of growth hormone during adipose cell differentiation is related to terminal events only and that its effects can be seen both at the protein and mRNA level. These results strongly suggest that an increased rate of specific transcription is primarily responsible for the accumulation of mRNAs during exposure to growth hormone.

scholarly journals Transcriptional Pausing Caused by NELF Plays a Dual Role in Regulating Immediate-Early Expression of the junB Gene

2006 ◽  
Vol 26 (16) ◽  
pp. 6094-6104 ◽  
Author(s):  
Masatoshi Aida ◽  
Yexi Chen ◽  
Koichi Nakajima ◽  
Yuki Yamaguchi ◽  
Tadashi Wada ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
Mrna Level ◽  
Proximal Region ◽  
Negative Regulation ◽  
Immediate Early ◽  
Dual Function ◽  
Early Expression ◽  
Transcriptional Pausing ◽  
Promoter Proximal Region

ABSTRACT Human 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole sensitivity-inducing factor (DSIF) and negative elongation factor (NELF) negatively regulate transcription elongation by RNA polymerase II (RNAPII) in vitro. However, the physiological roles of this negative regulation are not well understood. Here, by using a number of approaches to identify protein-DNA interactions in vivo, we show that DSIF- and NELF-mediated transcriptional pausing has a dual function in regulating immediate-early expression of the human junB gene. Before induction by interleukin-6, RNAPII, DSIF, and NELF accumulate in the promoter-proximal region of junB, mainly at around position +50 from the transcription initiation site. After induction, the association of these proteins with the promoter-proximal region continues whereas RNAPII and DSIF are also found in the downstream regions. Depletion of a subunit of NELF by RNA interference enhances the junB mRNA level both before and after induction, indicating that DSIF- and NELF-mediated pausing contributes to the negative regulation of junB expression, not only by inducing RNAPII pausing before induction but also by attenuating transcription after induction. These regulatory mechanisms appear to be conserved in other immediate-early genes as well.

Disruption of the vimentin intermediate filament system during adipose conversion of 3T3-L1 cells inhibits lipid droplet accumulation

1996 ◽  
Vol 109 (13) ◽  
pp. 3047-3058 ◽  
Author(s):  
J.G. Lieber ◽  
R.M. Evans
Keyword(s):  
Lipid Droplet ◽  
Lipid Droplets ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Marker Enzyme ◽  
C Cells ◽  
Pulse Label ◽  
Adipose Conversion ◽  
Glycerol 3 Phosphate Dehydrogenase ◽  
Vimentin Filaments

During the differentiation of 3T3-L1 pre-adipocytes, vimentin intermediate filaments are reorganized to form cage-like structures around the nascent lipid droplets. Initial studies with 3T3-L1 cells indicated that aggregation of vimentin filaments by nocodazole treatment during or shortly after induction of adipose conversion dramatically reduced the lipid droplet content of 3T3-L1 cells 96–120 hours after induction. Specific but transient disruption of vimentin following anti-IFA antibody injection also resulted in a decrease in lipid droplet formation in differentiating cells. To specifically and stably affect filament organization, 3T3-L1 cells lines were established by transfection with a glucocorticoid-regulatable, dominant negative mutant vimentin cDNA expression plasmid. Treatment of these cells (83 delta C) with dexamethasone resulted in expression of vimentin with a carboxyl-terminal deletion, which led to the disruption of the endogenous filament network. Induction of adipose conversion in 83 delta C cells lead to the formation of lipid droplets comparable to those seen in untransfected 3T3-L1 cells. Addition of dexamethasone during the adipose conversion of 83 delta C cells did not affect the induction of the marker enzyme glycerol-3-phosphate dehydrogenase or the incorporation of [14C]palmitate into triglycerides during a 10 minute pulse label. There was, however, a failure to form prominent lipid droplets and to accumulate [14C]palmitate-labeled triglycerides. Pulse-chase experiments indicated that the failure of these cells to accumulate triglyceride was associated with an increased rate of turnover. These studies indicate that vimentin filaments provide a function that influences lipid stability during adipose conversion of 3T3-L1 cells.

Coupling of growth arrest and expression of early markers during adipose conversion of preadipocyte cell lines

1986 ◽  
Vol 137 (2) ◽  
pp. 903-910 ◽  
Author(s):  
Ez-Zoubir Amri ◽  
Christian Dani ◽  
Alain Doglio ◽  
Paul Grimaldi ◽  
Gérard Ailhaud
Keyword(s):  
Cell Lines ◽  
Growth Arrest ◽  
Early Markers ◽  
Adipose Conversion

Expression and regulation of pOb24 and lipoprotein lipase genes during adipose conversion

1990 ◽  
Vol 43 (2) ◽  
pp. 103-110 ◽  
Author(s):  
C. Dani ◽  
E.-Z. Amri ◽  
B. Bertrand ◽  
S. Enerback ◽  
G. Bjursell ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Adipose Conversion

scholarly journals Id3 prevents differentiation of preadipose cells.

1997 ◽  
Vol 17 (4) ◽  
pp. 1796-1804 ◽  
Author(s):  
M Moldes ◽  
F Lasnier ◽  
B Fève ◽  
J Pairault ◽  
P Djian
Keyword(s):  
Cell Formation ◽  
Growth Arrest ◽  
Negative Regulator ◽  
Fat Cell ◽  
Viral Promoter ◽  
Helix Loop Helix ◽  
Fresh Serum ◽  
Fibroblast Line ◽  
Adipose Conversion ◽  
Adipose Differentiation

We have studied the expression of the Id1, Id2, and Id3 genes during adipose differentiation of 3T3-F442A cells. All three Id mRNAs are present in preadipose cells, but the mRNA for Id3 is the most abundant. All three Id mRNAs sharply decline in the course of adipose differentiation, and their virtual disappearance precedes differentiation. The decrease in Id2 and Id3 is associated with adipose differentiation rather than with growth arrest since it is not observed in 3T3-C2 cells, a fibroblast line with a very low susceptibility to adipose conversion. The decline in Id2 and Id3 mRNAs is associated with a reduced transcription rate of the two genes. Id1 mRNA is reduced in amount during adipose conversion of 3T3-F442A cells, but the decrease is also observed in resting 3T3-C2 cells and is associated with very little decrease in transcription of the gene. Addition of fresh serum reactivates Id3 gene expression in quiescent 3T3-C2 cells but not in adipose 3T3-F442A cells. Stably transformed preadipose cells expressing an Id3 cDNA under the control of a viral promoter are virtually unable to differentiate. We postulate that the Id3 protein is a negative regulator of fat cell formation and presumably acts by preventing an as yet unidentified basic helix-loop-helix protein from activating the program of differentiation.

scholarly journals Novel compounds that target lipoprotein lipase and mediate growth arrest in acute lymphoblastic leukemia

2018 ◽  
Vol 28 (10) ◽  
pp. 1937-1942
Author(s):  
Rajesh R. Nair ◽  
Werner J. Geldenhuys ◽  
Debbie Piktel ◽  
Prabodh Sadana ◽  
Laura F. Gibson
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Lipoprotein Lipase ◽  
Lymphoblastic Leukemia ◽  
Growth Arrest
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