scholarly journals Heritability of Transforming Growth Factor-β1 and Tumor Necrosis Factor-Receptor Type 1 Expression and Vitamin D Levels in Healthy Adolescent Twins

2014 ◽  
Vol 18 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Natalie T. Mills ◽  
Margie J. Wright ◽  
Anjali K. Henders ◽  
Darryl W. Eyles ◽  
Bernhard T. Baune ◽  
...  
Keyword(s):  
Vitamin D ◽  
Mental Illness ◽  
Growth Factor ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Tumor Necrosis Factor Receptor ◽  
Transforming Growth Factor Β1 ◽  
Healthy Adolescent ◽  
Necrosis Factor

Cytokines and vitamin D both have a role in modulating the immune system, and are also potentially useful biomarkers in mental illnesses such as major depressive disorder (MDD) and schizophrenia. Studying the variability of cytokines and vitamin D in a healthy population sample may add to understanding the association between these biomarkers and mental illness. To assess genetic and environmental contributions to variation in circulating levels of cytokines and vitamin D (25-hydroxy vitamin D: 25(OH)D3), we analyzed data from a healthy adolescent twin cohort (mean age 16.2 years; standard deviation 0.25). Plasma cytokine measures were available for 400 individuals (85 MZ, 115 DZ pairs), dried blood spot sample vitamin D measures were available for 378 individuals (70 MZ, 118 DZ pairs). Heritability estimates were moderate but significant for the cytokines transforming growth factor-β1 (TGF-β1), 0.57 (95% CI 0.26–0.80) and tumor necrosis factor-receptor type 1 (TNFR1), 0.50 (95% CI 0.11–0.63) respectively. Measures of 25(OH)D3 were within normal range and heritability was estimated to be high (0.86, 95% CI 0.61–0.94). Assays of other cytokines did not generate meaningful results. These potential biomarkers may be useful in mental illness, with further research warranted in larger sample sizes. They may be particularly important in adolescents with mental illness where diagnostic uncertainty poses a significant clinical challenge.

Expression of Tumor Necrosis Factor-α and Transforming Growth Factor-β1 in Acute Liver Injury

1989 ◽  
Vol 1 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Mark J. Czaja ◽  
Kathleen C. Flanders ◽  
Luis Biempica ◽  
Charna Klein ◽  
Mark A. Zern ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Acute Liver Injury ◽  
Transforming Growth Factor Β1 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals N6-Isopentenyladenosine promoted HeLa cell apoptosis through inhibitions of AKT and transforming growth factor β–activated kinase 1 activation

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769596 ◽  
Author(s):  
Miao Li ◽  
Yonghao Qi ◽  
Jing Wei ◽  
Lulu Lu ◽  
Xuan Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Cancer Cell ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Tumor Necrosis Factor Receptor ◽  
Transforming Growth Factor Β ◽  
Associated Factor ◽  
New Gene ◽  
Necrosis Factor

N6-Isopentenyladenosine, a member of the family of plant hormones, possesses anti-cancer activities on a number of cancer cell lines. However, its mode of action in cervical cancer cell remains poorly understood. Our computational docking studies showed that N6-Isopentenyladenosine could bind with the really interesting new gene domain of tumor necrosis factor receptor–associated factor 6, which is an ubiquitination E3 ligase. Tumor necrosis factor receptor–associated factor 6–mediated ubiquitination is known to activate both protein kinase B (also known as AKT) and transforming growth factor β–activated kinase 1, and the really interesting new gene domain comprises the core of the ubiquitin ligase catalytic domain. First, we evaluated the effects of iPA on cervical cancer cell line HeLa using MTT and flow cytometry. Second, we examined the effects of iPA on activation of tumor necrosis factor receptor–associated factor 6–mediated downstream targets using western blot or immunoprecipitation. iPA could reduce HeLa cell proliferation through apoptosis, and such anti-cancer activity is associated with inhibitions of both AKT and transforming growth factor β–activated kinase 1 signaling pathways. In addition, suppression of the anti-apoptotic protein Bcl-2 and elevation of the pro-apoptotic protein Bax were also observed. Anti-proliferation properties of iPA are likely due to its binding at the really interesting new gene domain of tumor necrosis factor receptor–associated factor 6 and loss of AKT and transforming growth factor β–activated kinase 1 activities as a result of functional modulations of tumor necrosis factor receptor–associated factor 6. These results support the emerging notion that tumor necrosis factor receptor–associated factor 6 could serve as a viable target for developing new cancer therapeutics.

Retroviral-Mediated Gene Transduction of c-kit Into Single Hematopoietic Progenitor Cells From Cord Blood Enhances Erythroid Colony Formation and Decreases Sensitivity to Inhibition by Tumor Necrosis Factor- and Transforming Growth Factor-β1

Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2319-2332 ◽  
Author(s):  
Li Lu ◽  
Michael C. Heinrich ◽  
Li-Sheng Wang ◽  
Mu-Shui Dai ◽  
Amy J. Zigler ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Progenitor Cells ◽  
Colony Formation ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Gm Csf ◽  
Cd34 Cells ◽  
Necrosis Factor

The c-kit receptor and its ligand, steel factor (SLF), are critical for optimal hematopoiesis. We evaluated effects of transducing cord blood (CB) progenitor cells with a retrovirus encoding humanc-kit cDNA. CD34+ cells were sorted as a population or as 1 cell/well for cells expressing high levels of CD34+++ and different levels of c-kit (++, +, Lo/−), transduced and then cultured in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, erythropoietin (Epo) +/− SLF in the absence of serum. At a single-cell level, transduction with c-kit, but not with control (neo only), virus significantly increased colony formation, especially by erythroid and multipotential progenitors. The enhancing effect of c-kit transduction was inversely correlated with expression of c-kit protein before transduction. The greatest enhancing effects were noted in CD34+++kitLo/− cells transduced with c-kit. The stimulating effect was apparent even in the absence of exogenously added SLF, but in the presence of GM-CSF, IL-3, IL-6, and Epo. Enzyme-linked immunosorbent assay (ELISA) of SLF protein, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of SLF mRNA expression in CD34+ cells, and use of neutralizing antibodies to SLF and/or c-kit suggested the presence of endogenous, although probably very low level, expression of SLF by these progenitor cells. Transduction of c-kit significantly decreased sensitivity of progenitor cells to the inhibitory effects of transforming growth factor-β1 and tumor necrosis factor-.c-kit–transduced cells had increased expression ofc-kit protein and decreased spontaneous or cytokine-induced apoptosis. Our results suggest that transduced c-kit into selected progenitor cells can enhance proliferation and decrease apoptosis and that endogenous SLF may mediate this effect.

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