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1. |
Granulocyte Colony-Stimulating Factor: Structure, Function and Physiology |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 179-186
LaytonJudith E.,
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ISSN:0897-7194
DOI:10.3109/08977199209026924
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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2. |
Clinical Applications of Granulocyte Colony Stimulating Factor (G-CSF) |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 187-191
GabriloveJanice Lynn,
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摘要:
AbstractThe production of neutrophil granulocytes is a complex and dynamic process during which a small number of limited stem cells give rise to lineage specific progenitors that proliferate in the bone marrow subsequently entering the blood as mature polymorphonuclear leukocytes. One hematopoietic growth factor which appears to specifically control the proliferation and terminal maturation of this specific myeloid lineage is granulocyte colony stimulating factor.
ISSN:0897-7194
DOI:10.3109/08977199209026925
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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3. |
Regulation of Expression of Transforming Growth Factor-β2 by Transforming Growth Factor-βIsoforms is Dependent upon Cell Type |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 193-201
O'reillyMichael A.,
DanielpourDavid,
RobertsAnita B.,
SpornMichael B.,
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摘要:
AbstractThe effect of three different isoforms of transforming growth factor-β(TGF-β) on the expression of TGF-β2 mRNA was studied in several continuous tumor cell lines. As previously reported for the mouse fibroblast cell line AKR-2B, the expression of TGF-β2 mRNA transcripts of 5.4, 4.7, 3.7 and 3.0 kb was decreased after a 24 hr treatment with 5ng/ml of TGF-β1, TGF-β2 or TGF-β3. In A549, HBL-100 and BSC-1 epithelial cell lines, five distinct TGF-β2 mRNA transcripts of 5.8, 5.1, 4.0, 3.8 and 2.8 kb were detected by Northern blot analysis. Treatment of these cells with TGF-β1, TGF-β2 or TGF-β3 for 24 hr resulted in a 2–3 fold increase in the 5.8, 4.0 and 3.8 kb transcripts, with little detectable change in abundance of the 5.1 and 2.8 kb transcripts. The effect of the TGF-βproteins was dose (5 ng/ml) and time (3–6 hr) dependent. A similar 2–3 fold increase in the level of secreted TGF-β2 was observed following treatment of A549 cells with TGF-β1. Basal level and induced expression of TGF-β2 mRNA in response to TGF-βisoforms was decreased in the presence of actinomycin D. In all cell lines studied, the expression of the 2.5 kb TGF-β1 mRNA was relatively unchanged or markedly increased in response to treatment with TGF-β. These studies support the hypothesis that expression of TGF-β2 is regulated by members of the TGF-βfamily and is dependent upon cell type.
ISSN:0897-7194
DOI:10.3109/08977199209026926
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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4. |
Distribution of Transforming Growth Factor Beta in a Two-Week-Old Human Embryo |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 203-208
PinarHalit,
ThompsonNancy L.,
FlandersKathleen C.,
SpornMichael B.,
SungJames,
RogersBeverly B.,
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摘要:
AbstractUsing inununohistochemical methods we have investigated the presence of transforming growth factorsβ1,β2 andβ1 precursor in a two-week-old trilaminar human embryo. TGF-β1 precursor was seen in both the epiblast and the hypoblast. In contrast to the widespread localization of TGF-β1 precursor in the embryo proper, antibodies to the mature TGF-β1 peptide localized preferentially to the hypoblast with only weak staining in the epiblast. Staining with antibodies to TGF-β2 was generally weak in both the epiblast and hypoblast layers of the embryo proper. These results show that TGF-β1 andβ2 peptides are detectable as early as the second week of human development.
ISSN:0897-7194
DOI:10.3109/08977199209026927
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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5. |
Molecular Cloning of CSF-1 Receptor from Rat Myoblasts. Sequence Analysis and Regulation During Myogenesis |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 209-218
GaëlleAnne,
GuillierMartine,
PierreMarie,
LeibovitchSerge Alexandre,
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摘要:
AbstractWe have isolated and sequenced a cDNA (mrfms) encoding rat c-fms gene (CSF-1 receptor) from proliferating L6α1 myoblasts. The predicted amino acid sequence was highly identical with the c-fms protein found in monocytes and macrophages (98, 76 and 84% identity from mouse, cat and human c-fms proteins, respectively). The mechanisms responsible for the regulation of mrfms gene expression during myogenesis were examined. Mrfms products were observed during proliferation of L6α1 myoblasts and were downregulated during differentiation. Run-on transcription assays demonstrated that the mrfms gene was transcriptionally active only in undifferentiated myoblasts. These findings suggested that mrfms levels in L6α1 myoblasts are controlled by transcriptional mechanisms. The half-life of mrfms transcripts was found to be at least 5 hr while inhibition of protein synthesis with cycloheximide (CHX) decreased this half-life to 30 min without changes in the rate of mrfms gene transcription. In addition oncogenic transformation of L6al myoblasts by the v-frns induced constitutive upregulation of mrfms mRNAs, and nuclear run-on assays demonstrated that mrfms transcription was not growth-factor dependent. Furthermore, these findings with others previously published indicate that mrfms gene products may play a role in the normal and neoplastic growth of muscular cells.
ISSN:0897-7194
DOI:10.3109/08977199209026928
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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6. |
The Expression of PDGFα- andβ-Receptors in Subpopulations of PDGF-Producing Cells Implicates Autocrine Stimulatory Loops in the Control of Proliferation in Cytotrophoblasts that Have Invaded the Maternal Endometrium |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 219-231
HolmgrenLars,
ClaessonLena,
HenrikCarl,
OhlssonRolf,
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摘要:
AbstractIn order to explain the high proliferative potential of human placental cytotrophoblasts, we have addressed the potential involvement of platelet-derived growth factor (PDGF) ligand and receptors. Although PDGF is usually described as a mitogen for cells of mesenchymal origin, we show in this report that extra-villous term placental cytotrophoblasts express the PDGFα- andβ-receptor genes, both in vivo and in vitro. In addition, cytotrophoblasts produce significant amounts of PDGF-B protein. By immunohistochemical analysis of receptor expression, we found that the PDGF a-receptors could be detected at the cell surface, while the PDGFβ-receptors were only detected inrracellularly. In addition, double immunostaining analysis showed that the PDGFα- andβ-receptor molecules are expressed in different subpopulations of cytotrophoblasts. The addition of PDGF-AA and PDGF-BB homodimers to cytotrophoblast primary cultures induced a significant increase in DNA synthesis. We conclude, therefore, that PDGF is a growth factor for placental cytotrophoblasts and suggest that the growth of cytotrophoblasts can partly be explained by a PDGF autostimulatory loop, limited by the number of receptor-positive cytotrophoblasts.
ISSN:0897-7194
DOI:10.3109/08977199209026929
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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7. |
Survival of the Myeloid Progenitor Cell Line FDC-P1 is Prolonged by Interferon-γor Interleukin-4 |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 233-242
KelsoAnne,
TrouttAnthony B.,
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摘要:
AbstractContinuous proliferation of the immortalized myeloid progenitor cell line FDC-P1 depends on stimulation with either interleukin-3 (IL-3) or granulocyte-macrophage colony stimulating factor (GM-CSF). Two other cytokines, interferon-γ(IFN-γ) and IL-4, were found to prolong FDC-P1 survival for several days. Surviving cells incorporated [3H]thymidine and a minority completed up to 3 cell divisions before dying. This transient proliferative response was a direct effect of IFN-γand IL-4 since these cytokines did not induce production of detectable IL-3 or GM-CSF and the response was unaffected by cell concentration. IL-6, a constitutive product of FDC-P1 cells whose secretion was increased by IL-3, GM-CSF and IL-4 but not by IFN-γ, was not responsible for the proliferative response. FDC-P1 lines that constirutively expressed the cell cycle-associated oncogene myc or the survival-associated oncogene bcl-2 also responded only transiently to IFN-γor IL-4, indicating that expression of these genes did not complement the signals delivered by IFN-γor IL-4. By contrast, the protein kinase C activator phorbol 12-myristate 13-acetate (PMA) prolonged survival of FDC-P1 cells on its own and potentiated the response to IFN-γor IL-4, although the combination of stimuli did not support long-term growth. It is concluded that IFN-γand IL-4 trigger only some of the signalling events that lead to mitogenesis; these events are complemented by stimulation with PMA but additional signals are required for sustained proliferation.
ISSN:0897-7194
DOI:10.3109/08977199209026930
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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8. |
Effects of Epidermal Growth Factor on Calf Renal Glomerular Cells In Vitro |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 243-254
TassinM. T.,
BoyerB.,
SichM.,
GuicharnaudL.,
DerisY.,
GublerM. C.,
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摘要:
AbstractEpidermal growth factor (EGF) stimulates the mitosis and differentiation of a variety of cellular types. It also delays the cell senescence in vitro. Because of its multiple functions, the effects of EGF on cells from isolated, explanted calf renal glomeruli have been studied. The cell types emerging from glomeruli cultured with and without EGF were compared and identified by morphological, immunofluorescence and electron microscopy criteria. Two cell types: visceral epithelial cells or podocytes (type I) and mesangial cells (type II) emerged from glomeruli cultivated without EGF. A third cell type, called type III cells, appeared only in the presence of EGF. These cells divided, were mobile and had prolonged lifespan in culture. They appeared pavement-like, and acquired progressively the morphological features and cytoskeletal components of type I cells. They also showed certain characteristics of podocytes in vivo. We suggest that type III epithelial-like cells are precursor cells of podocytes, that EGF triggers their emergence from glomeruli and their subsequent proliferation and differentiation in vitro. EGF also prolongs their lifetime in culture.
ISSN:0897-7194
DOI:10.3109/08977199209026931
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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9. |
Terminal Differentiation of Mouse Preadipocyte Cells: The Mitogenic-Adipogenic Role of Growth Hormone is Mediated by the Protein Kinase C Signalling Pathway |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 255-264
MarieRose,
GaillardDanielle,
AilhaudGÉRard,
NégrelRaymond,
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摘要:
AbstractThe role of growth hormone (GH) in the differentiation process of Obi 771 mouse preadipocyte cells has been studied under culture conditions that were serum-free and hormone-supplemented and which were previously shown to lead to terminal differentiation. In the absence of GH, a dramatic decrease in the adipogenic activity of the culture medium could be observed, as indicated 12 days after confluence by the low levels of glycerol-3-phosphate dehydrogenase activity and the sharp reduction of the number of triacylglycerol-containing cells. This decrease in adipogenic activity was accompanied by a parallel loss of the mitogenic potency of the culture medium. Determination of the half-maximal and maximal concentrations of GH required for the restoration of growth and differentiation were identical, 0.5 and 2 nM, respectively. Despite the presence of insulin-like growth factor-I (IGF-I) to substitute for supraphysiological concentrations of insulin and to saturate IGF-I receptor, GH was still required to induce terminal differentiation of a maximal number of cells. However, protein kinase C activators such as prostaglandin F2a, phorbol esters and diacylglycerol were able to mimic GH in promoting a maximal mitogenic-adipogenic response, indicating that the ability of GH to induce diacylglycerol production (Doglio et al., 1989; Catalioto et al., 1990) plays a prominent role in this process. Furthermore, in agreement with the fact that the mitoses which precede terminal differentiation of Obi 771 preadipocytes are strictly controlled by cAMP and only modulated by protein kinase C., terminal differentiation of Ob 1771 preadipocytes occured in the absence of GH upon supplementation with high concentrations of carbaprostacyclin, added as a cAMP-elevating agent or with 8-Br-cAMP, added as a cAMP analogue. It is concluded that the control exerted by GH on terminal differentiation of mouse preadipocytes corresponds to a modulating mitogenic effect mediated through protein kinase C activation and leading to a potentiation of the cAMP and IGF-I mitogenic signalling pathways.
ISSN:0897-7194
DOI:10.3109/08977199209026932
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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10. |
Transforming Growth Factor Beta Stimulates Mitogenically Mouse NIH3T3 Fibroblasts and Those Cells Transformed by the EJ-H-ras Oncogene |
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Growth Factors,
Volume 6,
Issue 3,
1992,
Page 265-275
BenzakourOmar,
MerzakAbderrahim,
DoogheYolande,
PironinMartine,
LawrenceDavid,
VigierPhilippe,
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摘要:
AbstractTGF-β1 stimulates thymidine incorporation and the growth rate of mouse NIH3T3 fibroblasts and of those cells transformed by the EJ-H-ras oncogene (TR15 cells), in the presence and the absence of serum. Thymidine incorporation, in serum-deprived cells, is stimulated to a higher degree by 0.1-1 ng/ml of TGF-βin NIH3T3 than in TR15 cells, which have a 10-fold higher basal level of incorporation. In both cell types TGF-β1 is as active, or more active than other mitogens (TGF-α, PDGF-AB, bFGF) at the same concentration. The growth rate of NIH3T3 cells, in low serum or serum-free (S−) medium, is stimulated by only 10 picograms/ml of TGF-β1, and that of TR15 cells, in S−medium, by only 1 picogram/m1. In contrast, TGF-β1 inhibits mitogenically unestablished mouse embryo fibroblasts and these fibroblasts immortalized spontaneously and able to grow in S−medium. It also inhibits the anchorage-independent growth of TR15 cells. NIH3T3 and TR15 cells respond, similarly, to TGF-βactivated by acification of their culture medium. The kinetics of thymidine incorporation and of activation of the c-myc proto-oncogene, observed already after 1 hr, in treated NIH3T3 and TR15 cells, suggests a direct mitogenic stimulation. The level of activated c-myc RNA is 2-fold higher at 2 hr, and subsequently decreases relatively less in the TR15 cells.
ISSN:0897-7194
DOI:10.3109/08977199209026933
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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