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211.
Tiziano Baroni Catia Bellucci Cinzia Lilli Furio Pezzetti Francesco Carinci Eleonora Lumare Annalisa Palmieri Giordano Stabellini Maria Bodo 《Journal of cellular physiology》2010,222(3):748-756
Nonsyndromic cleft lip with or without cleft palate (CLP) is a frequent craniofacial malformation caused by both genetic and environmental factors. Maternal smoking during pregnancy is a known risk factor, due to the teratogenic role of nicotine. To assess and compare the impact of CLP and nicotine, we studied the quantitative expression of genes involved in signaling pathways and extracellular matrix (ECM) metabolism in human normal nicotine‐treated (NicN) and CLP fibroblasts compared to normal control (CTRL) cells. Palatal fibroblast cultures from seven CLP children and seven age‐matched CTRL subjects were established and subconfluent cells incubated for 24 h without (CTRL and CLP fibroblasts) or with (NicN fibroblasts) 0.6 mM nicotine. Gene expressions were analyzed by real‐time quantitative PCR. For the first time, a regulated cholinergic signaling in our human fibroblasts in vitro was demonstrated. Members of TGF‐beta, retinoic acid (RA), and GABA‐ergic signaling systems were also differently regulated. Among the ECM genes, fibronectin, syndecan, integrin α2, and MMP13 genes were concordantly modulated, while integrin β5, and decorin genes were discordantly modulated. Interestingly, nicotine treatment regulated gene expressions of CD44 and CLPTM1, two candidate genes for CLP. Our findings show a positive association between nicotine treatment and CLP phenotype. Results suggest that nicotine deranges normal palate development, which might contribute to the development of a CLP malformative phenotype, through the impairment of some important signaling systems and ECM composition. J. Cell. Physiol. 222: 748–756, 2010. © 2009 Wiley‐Liss, Inc. 相似文献
212.
Catia Andreassi Raphaëlle Luisier Hamish Crerar Marousa Darsinou Sasja Blokzijl-Franke Tchern Lenn Nicholas M. Luscombe Giovanni Cuda Marco Gaspari Adolfo Saiardi Antonella Riccio 《Cell reports》2021,34(8):108778
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213.
Melissa Cavalheiro Tourino Edson Mendes de Oliveira Luziane Potrich Bellé Franciele Hinterholz Knebel Renata Chaves Albuquerque Felipe Augusto Dörr Sabrina Sayori Okada Silene Migliorini Irene Silva Soares Ana Campa 《Cell biochemistry and function》2013,31(5):361-364
Indoleamine 2,3‐dioxygenase (IDO) is an interferon‐γ (IFN‐γ)–induced tryptophan‐degrading enzyme, producing kynurenine (KYN) that participates in the mechanism of tumor immune tolerance. Thus, IDO inhibition has been considered a strategy for anticancer therapy. The aim of this study was to identify whether the metabolites originated from the competitive routes of tryptophan metabolism, such as the serotonergic or N, N‐dimethyltryptamine (DMT) pathways, have inhibitory effects on recombinant human IDO (rhIDO) activity. Serotonin and melatonin had no effect; on the other hand, tryptamine (TRY) and DMT modulated the activity of rhIDO as classical non‐competitive inhibitors, with Ki values of 156 and 506 μM, respectively. This inhibitory effect was also observed on constitutively expressed or IFN‐γ–induced IDO in the A172 human glioma cell line. TRY and DMT increased the cytotoxic activity of peripheral blood mononuclear cells (PBMCs) in co‐culture assays. We conclude that the IDO inhibition by TRY and DMT contributed to a more effective tumor‐reactive response by the PBMCs. Copyright © 2013 John Wiley & Sons, Ltd. 相似文献
214.
Submitochondrial particles were fused with purple membranes of Halobacterium halobium cells by means of a freeze-thawe sonication procedure. It is reported that fusion of inner mitochondrial membranes with a bacterial membrane yields a new particle which shows not only retention of redox- and photon-linked energy-coupling activities, but also creation of an additional energy-coupling process, light-driven ATP synthesis. 相似文献