scholarly journals Wound-factor-induced and cell cycle phase-dependent expression of 9E3/CEF4, the avian gro gene.

1991 ◽  
Vol 2 (9) ◽  
pp. 739-752 ◽  
Author(s):  
M Martins-Green ◽  
C Tilley ◽  
R Schwarz ◽  
C Hatier ◽  
M J Bissell
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Cell Damage ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Dependent Manner ◽  
Normal Tissues ◽  
Serum Stimulation

The gro genes encode for secreted proteins with sequence homologies to inflammatory mediators. Little is known about the function of these proteins or their regulation. The chicken gro (9E3/CEF4) is expressed abundantly in the cells of proliferating cultures but at very low levels in confluent cultures. In vivo, this gene is expressed in connective tissue and overexpressed at sites of injury, especially in areas of neovascularization. Here we provide a bridge between these observations by examining in culture the effect on 9E3 expression and DNA synthesis induced by cell damage and by addition of factors known to be released on wounding. We mimicked wounding by scraping swaths across confluent cultures of embryonic fibroblasts and determined the time dependence of expression of 9E3 mRNA and incorporation of 3H-thymidine. We find that 9E3 is (1) transiently expressed after "wounding" or serum-stimulation; (2) expressed in a cell cycle phase-dependent manner; it is triggered during the G0-G1 transition or early in G1 and subsides during S-phase; and (3) stimulated to high levels by a-fibroblast growth factor (aFGF), bFGF, transforming growth factor alpha (TGF alpha), and TGF beta, to intermediate levels by platelet-derived growth factor and not stimulated by epidermal growth factor. We also find that cells that are constantly cycling do not express 9E3, indicating that they skip either the portion of the cell cycle where 9E3 is induced or that they constitutively express a repressor of transcription or an RNA-degrading enzyme. Taken together, these observations suggest that the product of this gene could play more than one role in vivo. For example, in normal tissues the 9E3 protein could be involved in the exit of cells from the resting stage, whereas during wound healing the secreted protein or its cleavage products also could play a role in angiogenesis.

Abstract 18267: Effect of the Stress by Supercooling on Cell Proliferation and Immunogenicity of Transplanted Human Induced Pluripotent Stem (iPS) Derived Cardiomyoctes

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hisashi Moriguchi
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Growth Curves ◽  
Peripheral Blood Lymphocytes ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Control Group ◽  
Heart Cells ◽  
Induced Pluripotent

BACKGROUND: Cell preservation is essential for cell transplantation. I examined the effects of the stress by supercooling on the transplantation of human induced pluripotent stem (iPS) derived cardiomyoctes. METHODS: Human iPS derived cardiomyoctes were cultured for 20 days (control group), cryopreserved by supercooling macine for 1 week, and rapidly thawed and cultured for 20 days. Proliferation was compared among control and cryopreserved human iPS derived cardiomyoctes by constructing growth curves. Growth factors, cytokines, biochemical features, and cell cycle phase were measured immediately before and after cryopreservation by supercooling, and immunogenicity was evaluated from growth curves generated from human iPS derived cardiomyoctes after 7 days in mixed-lymphocyte culture. Control or cryopreserved human iPS derived cardiomyoctes were transplanted into pig connective tissues and evaluated histologically 2 weeks later. RESULTS: Cryopreserved human iPS derived cardiomyoctes proliferated more effectively than control cells (P<0.001). Levels of basic fibroblast growth factor and transforming growth factor-β1 were significantly higher (P<0.001), and those of interleukin (IL)-6 and IL-8 were significantly lower after cryopreservation (P<0.001). Fewer peripheral blood lymphocytes were produced in cryopreserved cells than in noncryopreserved cells (P=0.01), and the cell cycle phase of cryopreserved human iPS derived cardiomyoctes shifted primarily to G2 + M from G1 + G0. Noncryopreserved and cryopreserved human iPS derived cardiomyoctes both survived in connective tissue. CONCLUSION: The stress by supercooling can increase the proliferation of human iPS derived cardiomyoctes and also reduce the immunogenicity of the human heart cells.

scholarly journals CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor–β–dependent manner

2005 ◽  
Vol 202 (8) ◽  
pp. 1075-1085 ◽  
Author(s):  
François Ghiringhelli ◽  
Cédric Ménard ◽  
Magali Terme ◽  
Caroline Flament ◽  
Julien Taieb ◽  
...  
Keyword(s):  
Growth Factor ◽  
Natural Killer ◽  
Cell Activation ◽  
Transforming Growth Factor ◽  
Nk Cell ◽  
Killer Cell ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Cell Functions

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, reduced NKG2D receptor expression, and accelerated the growth of tumors that are normally controlled by NK cells. Conversely, the depletion of mouse T reg cells exacerbated NK cell proliferation and cytotoxicity in vivo. Human NK cell–mediated tumor recognition could also be restored by depletion of T reg cells from tumor-infiltrating lymphocytes. These findings support a role for T reg cells in blunting the NK cell arm of the innate immune system.

scholarly journals Heterogeneous Nuclear Ribonucleoprotein C Modulates Translation of c-myc mRNA in a Cell Cycle Phase-Dependent Manner

2003 ◽  
Vol 23 (2) ◽  
pp. 708-720 ◽  
Author(s):  
Jong Heon Kim ◽  
Ki Young Paek ◽  
Kobong Choi ◽  
Tae-Don Kim ◽  
Bumsuk Hahm ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Phase ◽  
In Vitro Translation ◽  
Cycle Phase ◽  
Dependent Manner ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
M Phase ◽  
Hnrnp C ◽  
A Cell ◽  
Nuclear Ribonucleoprotein

ABSTRACT The c-myc proto-oncogene plays a key role in the proliferation, differentiation, apoptosis, and regulation of the cell cycle. Recently, it was demonstrated that the 5′ nontranslated region (5′ NTR) of human c-myc mRNA contains an internal ribosomal entry site (IRES). In this study, we investigated cellular proteins interacting with the IRES element of c-myc mRNA. Heterogeneous nuclear ribonucleoprotein C (hnRNP C) was identified as a cellular protein that interacts specifically with a heptameric U sequence in the c-myc IRES located between two alternative translation initiation codons CUG and AUG. Moreover, the addition of hnRNP C1 in an in vitro translation system enhanced translation of c-myc mRNA. Interestingly, hnRNP C was partially relocalized from the nucleus, where most of the hnRNP C resides at interphase, to the cytoplasm at the G2/M phase of the cell cycle. Coincidently, translation mediated through the c-myc IRES was increased at the G2/M phase when cap-dependent translation was partially inhibited. On the other hand, a mutant c-myc mRNA lacking the hnRNP C-binding site, showed a decreased level of translation at the G2/M phase compared to that of the wild-type message. Taken together, these findings suggest that hnRNP C, via IRES binding, modulates translation of c-myc mRNA in a cell cycle phase-dependent manner.

Sign in / Sign up

Export Citation Format

Share Document