keyword
https://read.qxmd.com/read/15459768/involvement-of-growth-differentiation-factor-15-macrophage-inhibitory-cytokine-1-gdf-15-mic-1-in-oxldl-induced-apoptosis-of-human-macrophages-in-vitro-and-in-arteriosclerotic-lesions
#21
JOURNAL ARTICLE
Daniel Schlittenhardt, Andreas Schober, Jens Strelau, Gabriel A Bonaterra, Walther Schmiedt, Klaus Unsicker, Jürgen Metz, Ralf Kinscherf
Growth differentiation factor-15/macrophage inhibitory cytokine-1 (GDF-15/MIC-1) is a new member of the transforming growth factor beta (TGF-beta) superfamily, which has most recently been found in activated macrophages (MPhi). We have now investigated GDF-15/MIC-1 in human MPhi after exposure to oxidized low-density lipoproteins (oxLDL) related mediators in vitro and in arteriosclerotic carotid arteries. Using RT-PCR and Western blotting a pronounced induction of GDF-15/MIC-1 expression by oxLDL, C6-ceramide, tumor necrosis factor (TNFalpha) and hydrogen peroxide (H2O2) was found in cultured human MPhi...
November 2004: Cell and Tissue Research
https://read.qxmd.com/read/12832851/prostaglandin-f2alpha-induced-functional-regression-of-the-corpus-luteum-and-apoptosis-in-rodents
#22
JOURNAL ARTICLE
Zhiyan Wang, Kazuhiro Tamura, Mikihiro Yoshie, Hiroshi Tamura, Kazuhiko Imakawa, Hiroshi Kogo
We investigated the relationship between prostaglandin (PG) F(2)(alpha)-induced functional luteal regression and apoptosis in the rodent ovary. Administration of PGF(2)(alpha) significantly decreased the serum levels of progesterone within 12 h after treatment in pseudopregnant mice. Apparent signals were detected in luteal tissues at 24 to 72 h by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick endo labeling (TUNEL) assay. PGF(2)(alpha) significantly increased the levels of the cleavage nuclear poly (ADP-ribose) polymerase fragment and transforming growth factor-beta (TGF-beta) mRNA within 48 h...
May 2003: Journal of Pharmacological Sciences
https://read.qxmd.com/read/12728250/tgf-beta1-suppresses-apoptosis-via-differential-regulation-of-map-kinases-and-ceramide-production
#23
JOURNAL ARTICLE
H-H Chen, S Zhao, J-G Song
Serum deprivation induces apoptosis in NIH3T3 cells, which is associated with increased intracellular ceramide generation and with the activation of p38 mitogen-activated protein (MAP) kinase. Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis...
May 2003: Cell Death and Differentiation
https://read.qxmd.com/read/12515830/modulation-of-transforming-growth-factor-beta-tgf-beta-signaling-by-endogenous-sphingolipid-mediators
#24
JOURNAL ARTICLE
Madoka Sato, Margaret Markiewicz, Masoyoshi Yamanaka, Alicja Bielawska, Cungui Mao, Lina M Obeid, Yusuf A Hannun, Maria Trojanowska
Transforming growth factor-beta (TGF-beta) is a multifunctional growth factor that plays a critical role in tissue repair and fibrosis. Sphingolipid signaling has been shown to regulate a variety of cellular processes and has been implicated in collagen gene regulation. The present study was undertaken to determine whether endogenous sphingolipids are involved in the TGF-beta signaling pathway. TGF-beta treatment induced endogenous ceramide levels in a time-dependent manner within 5-15 min of cell stimulation...
March 14, 2003: Journal of Biological Chemistry
https://read.qxmd.com/read/12219934/paradoxical-effects-of-tumour-necrosis-factor-alpha-on-rat-granulosa-cell-dna-synthesis
#25
COMPARATIVE STUDY
Guillermo M Lanuza, Patricia E Saragüeta, Ursula A Bussmann, J Lino Barañao
Tumour necrosis factor-alpha (TNF-alpha) has been proposed as an intraovarian modulator of granulosa cell function. The effect of TNF-alpha on DNA synthesis in cultured rat granulosa cells was examined. Tumour necrosis factor-alpha stimulated thymidine incorporation when added in the presence of transforming growth factor-beta (TGF-beta). In contrast, the co-mitogenic effect of follicle-stimulating hormone (FSH) and TGF-beta was inhibited in a dose-dependent manner by TNF-alpha. Inhibition of FSH-dependent DNA synthesis by TNF-alpha was also found when cultures were co-stimulated with activin A...
2002: Reproduction, Fertility, and Development
https://read.qxmd.com/read/12085194/differential-interactions-between-igfbp-3-and-transforming-growth-factor-beta-tgf-beta-in-normal-vs-cancerous-breast-epithelial-cells
#26
COMPARATIVE STUDY
C McCaig, C A Fowler, N J Laurence, T Lai, P B Savage, J M P Holly, C M Perks
In addition to modulating insulin-like growth factors action, it is now clear that insulin-like growth factor-binding protein-3 also has intrinsic effects on cell growth and survival. We have compared the effects of insulin-like growth factor-binding protein-3 and transforming growth factor-beta on cell proliferation and death of Hs578T cells and the normal breast epithelial cell line, MCF-10A. The growth of MCF-10A cells was inhibited at low concentrations of insulin-like growth factor-binding protein-3 but stimulated at high concentrations...
June 17, 2002: British Journal of Cancer
https://read.qxmd.com/read/11741524/cycloheximide-blocks-tgf-beta1-induced-apoptosis-in-murine-hepatocytes
#27
JOURNAL ARTICLE
J H Liao, B H Zhou, M Q Chai, J G Song
AIM: To study the mechanism of transforming growth factor beta1-induced apoptosis in cultured hepatocytes. METHODS: DNA fragmentation and fluorescent microscopy were used to characterize cell apoptosis. Crystal violet staining was used to assess cell viability. Immunoblotting was used to detect Tak1, p53, and Bax. Dual luciferase assay was used to determine TGF-beta1-induced gene expression. Thin layer chromatography was used to examine ceramide level in AML12 cells...
February 2001: Acta Pharmacologica Sinica
https://read.qxmd.com/read/11668037/dominant-negative-tak1-induces-c-myc-and-g-0-exit-in-liver
#28
JOURNAL ARTICLE
C A Bradham, E Hatano, D A Brenner
Transforming growth factor-beta (TGF-beta)-activated kinase 1 (TAK1), a serine/threonine kinase, is reported to function in the signaling pathways of TGF-beta, interleukin 1, and ceramide. However, the physiological role of TAK1 in vivo is largely unknown. To assess the function of TAK1 in vivo, dominant-negative TAK1 (dnTAK1) was expressed in the rat liver by adenoviral gene transfer. dnTAK1 expression abrogated c-Jun NH(2)-terminal kinase and c-Jun but not nuclear factor (NF)-kappaB or SMAD activation after partial hepatectomy (PH)...
November 2001: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://read.qxmd.com/read/11532859/ras-oncogene-expression-determines-sensitivity-for-intercellular-induction-of-apoptosis
#29
JOURNAL ARTICLE
A Schwieger, L Bauer, J Hanusch, C Sers, R Schäfer, G Bauer
Fibroblasts carrying an inducible ras oncogene acquire the transformed phenotype after oncogene induction. As a consequence, the transformed cells become sensitive to intercellular induction of apoptosis, a novel regulatory process directed by non-transformed fibroblasts against their transformed descendants. The causal relationship between oncogene expression and sensitivity to intercellular induction of apoptosis is based on extracellular superoxide anion production by oncogene-expressing cells. Superoxide anions (after dismutation to hydrogen peroxide) thereby foster HOCl synthesis and at the same time direct the selectivity of apoptosis induction through hydroxyl generation from HOCl...
September 2001: Carcinogenesis
https://read.qxmd.com/read/11160743/activators-of-the-epstein-barr-virus-lytic-program-concomitantly-induce-apoptosis-but-lytic-gene-expression-protects-from-cell-death
#30
JOURNAL ARTICLE
G J Inman, U K Binné, G A Parker, P J Farrell, M J Allday
Expression of the lytic cycle genes of Epstain-Barr virus (EBV) is induced in type I Burkitt's lymphoma-derived cells by treatment with phorbol esters (e.g., phorbol myristate acetate [PMA]), anti-immunoglobulin, or the cytokine transforming growth factor beta (TGF-beta). Concomitantly, all these agents induce apoptosis as judged by a sub-G1 fluorescence-activated cell sorter (FACS) profile, proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining...
March 2001: Journal of Virology
https://read.qxmd.com/read/10936067/apoptosis-and-the-liver
#31
REVIEW
S Kanzler, P R Galle
Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for survival...
June 2000: Seminars in Cancer Biology
https://read.qxmd.com/read/10861856/tgf-beta-signaling-in-a549-lung-carcinoma-cells-lipid-second-messengers
#32
JOURNAL ARTICLE
R A Ignotz, T Honeyman
Transforming growth factor-beta (TGF-beta) is a potent inducer of numerous extracellular matrix components, largely through a transcriptional mechanism. To define the postreceptor signaling pathways used by TGF-beta in the induction of extracellular matrix gene expression, we have utilized the human lung carcinoma cell line, A549, in transfection experiments with the TGF-beta inducible reporter construct, p3TP-Lux. Previous work from this laboratory using pharmacologic agents suggested that a phosphatidylcholine-specific phospholipase C and protein kinase C may be involved in early aspects of TGF-beta signaling...
June 12, 2000: Journal of Cellular Biochemistry
https://read.qxmd.com/read/9581540/transforming-growth-factor-beta1-attenuates-ceramide-induced-cpp32-yama-activation-and-apoptosis-in-human-leukaemic-hl-60-cells
#33
JOURNAL ARTICLE
M L Kuo, C W Chen, S H Jee, S E Chuang, A L Cheng
Ceramide, a product of sphingomyelin turnover, is a novel lipid second messenger that mediates important cellular functions including proliferation, differentiation and apoptosis. This study demonstrates that the CPP32/Yama protease was activated during apoptosis induced by the membrane-permeable second messenger C2-ceramide in HL-60 cells. We also found that the addition of a specific tetrapeptide inhibitor of CPP32/Yama, Ac-DEVD-CHO, provided an effective protection against ceramide-induced cell death. These results suggested that CPP32/Yama has a central role in ceramide-mediated apoptosis...
November 1, 1997: Biochemical Journal
https://read.qxmd.com/read/9547591/the-rise-and-fall-of-ceramide-and-1-2-diacylglycerol-dag-modulation-by-transforming-growth-factor-beta-1-tgf-beta-1-and-by-epidermal-growth-factor-egf
#34
JOURNAL ARTICLE
T Goldkorn, T Ding
Transforming growth factor beta 1 (TGF beta 1) increases the phosphorylation of the epidermal growth factor (EGF) receptor and inhibits the growth of A431 cells, but the mechanism of TGF beta 1 signaling is unknown. Recent studies from this and other laboratories suggest a novel sphingomyelin signal transduction pathway (1-4). Ceramide, which is generated by sphingomyelinase action, can be deacylated to sphingoid bases, which are potential inhibitors of protein kinase C (PKC). Ceramide appears to have bioeffector properties...
1997: Advances in Experimental Medicine and Biology
https://read.qxmd.com/read/9449644/tumor-necrosis-factor-ceramide-transforming-growth-factor-beta1-and-aging-reduce-na-i-symporter-messenger-ribonucleic-acid-levels-in-frtl-5-cells
#35
JOURNAL ARTICLE
A E Pekary, J M Hershman
Iodide uptake, which is necessary for thyroid hormone synthesis, can be inhibited by aging, withdrawal of TSH, or increased tumor necrosis factor (TNF) and transforming growth factor (TGF)-beta1 levels resulting from the nonthyroid illness syndrome. TNF induces receptor-mediated activation of sphingomyelinase, which converts sphingomyelin to ceramide, a mediator of TNF actions. Thyroid follicular cells transport iodide from blood into the follicular lumen against an iodide gradient by means of coupled transport of Na+ ions and I- ions via the Na+/I- symporter (NIS)...
February 1998: Endocrinology
https://read.qxmd.com/read/9292957/sphingomyelinase-and-phospholipase-a2-regulate-type-i-deiodinase-expression-in-frtl-5-cells
#36
JOURNAL ARTICLE
A E Pekary, I J Chopra, L Berg, J M Hershman
We have previously reported (Mol. Cell. Endocrinol. (1994) 101, R31-R35) that the proinflammatory cytokines, tumor necrosis factor-alpha (TNF), interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma), have a marked inhibitory effect on the expression and activity of type I iodothyronine deiodinase (D1) in FRTL-5 rat thyroid cells, while the anti-inflammatory cytokine, transforming growth factor-beta 1 (TGF-beta 1) had no effect. These three proinflammatory cytokines utilize a number of intracellular second messenger systems including the pathways beginning with activation of sphingomyelinase and phospholipase A2...
August 1997: Thyroid: Official Journal of the American Thyroid Association
https://read.qxmd.com/read/9121342/regulation-of-muscarinic-m2-receptors
#37
REVIEW
P J Barnes, E B Haddad, J Rousell
The molecular mechanisms involved in the regulation of muscarinic receptor gene expression are poorly understood. In an effort to gain a better understanding of the regulation of M2 receptors, we have investigated homologous and heterologous regulation of M2 muscarinic receptor protein and gene expression in human embryonic lung fibroblasts (HEL 299 cells). HEL 299 cells constitutively express m2 receptors, with no evidence of other muscarinic receptor subtypes. We have shown that M2 receptors in these cells can be down-regulated by muscarinic and beta2-adrenergic receptor agonists...
1997: Life Sciences
https://read.qxmd.com/read/9063586/cellular-signaling-roles-of-tgf-beta-tnf-alpha-and-beta-app-in-brain-injury-responses-and-alzheimer-s-disease
#38
REVIEW
M P Mattson, S W Barger, K Furukawa, A J Bruce, T Wyss-Coray, R J Mark, L Mucke
beta-Amyloid precursor protein (beta APP), transforming growth factor beta (TGF beta), and tumor necrosis factor-alpha (TNF alpha) are remarkably pleiotropic neural cytokines/neurotrophic factors that orchestrate intricate injury-related cellular and molecular interactions. The links between these three factors include: their responses to injury; their interactive effects on astrocytes, microglia and neurons; their ability to induce cytoprotective responses in neurons; and their association with cytopathological alterations in Alzheimer's disease...
February 1997: Brain Research. Brain Research Reviews
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