共查询到20条相似文献,搜索用时 8 毫秒
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Jinyoung Son Misun Kim Ilo Jou Kyoung Chan Park Hee Young Kang 《Pigment cell & melanoma research》2014,27(2):201-208
Inflammatory cytokines are closely related to pigmentary changes. In this study, the effects of IFN‐γ on melanogenesis were investigated. IFN‐γ inhibits basal and α‐MSH‐induced melanogenesis in B16 melanoma cells and normal human melanocytes. MITF mRNA and protein expressions were significantly inhibited in response to IFN‐γ. IFN‐γ inhibited CREB binding to the MITF promoter but did not affect CREB phosphorylation. Instead, IFN‐γ inhibited the association of CBP and CREB through the increased association between CREB binding protein (CBP) and STAT1. These findings suggest that IFN‐γ inhibits both basal and α‐MSH‐induced melanogenesis by inhibiting MITF expression. The inhibitory action of IFN‐γ in α‐MSH‐induced melanogenesis is likely to be associated with the sequestration of CBP via the association between CBP and STAT1. These data suggest that IFN‐γ plays a role in controlling inflammation‐ or UV‐induced pigmentary changes. 相似文献
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Xiaohui Yu Baoyin Jia Faqiang Wang Xiuxiu Lv Xuemei Peng Yiyang Wang Hongmei Li Yanping Wang Daxiang Lu Huadong Wang 《Journal of cellular and molecular medicine》2014,18(2):263-273
Cardiomyocyte tumour necrosis factor α (TNF‐α) production contributes to myocardial depression during sepsis. This study was designed to observe the effect of norepinephrine (NE) on lipopolysaccharide (LPS)‐induced cardiomyocyte TNF‐α expression and to further investigate the underlying mechanisms in neonatal rat cardiomyocytes and endotoxaemic mice. In cultured neonatal rat cardiomyocytes, NE inhibited LPS‐induced TNF‐α production in a dose‐dependent manner. α1‐ adrenoceptor (AR) antagonist (prazosin), but neither β1‐ nor β2‐AR antagonist, abrogated the inhibitory effect of NE on LPS‐stimulated TNF‐α production. Furthermore, phenylephrine (PE), an α1‐AR agonist, also suppressed LPS‐induced TNF‐α production. NE inhibited p38 phosphorylation and NF‐κB activation, but enhanced extracellular signal‐regulated kinase 1/2 (ERK1/2) phosphorylation and c‐Fos expression in LPS‐treated cardiomyocytes, all of which were reversed by prazosin pre‐treatment. To determine whether ERK1/2 regulates c‐Fos expression, p38 phosphorylation, NF‐κB activation and TNF‐α production, cardiomyocytes were also treated with U0126, a selective ERK1/2 inhibitor. Treatment with U0126 reversed the effects of NE on c‐Fos expression, p38 mitogen‐activated protein kinase (MAPK) phosphorylation and TNF‐α production, but not NF‐κB activation in LPS‐challenged cardiomyocytes. In addition, pre‐treatment with SB202190, a p38 MAPK inhibitor, partly inhibited LPS‐induced TNF‐α production in cardiomyocytes. In endotoxaemic mice, PE promoted myocardial ERK1/2 phosphorylation and c‐Fos expression, inhibited p38 phosphorylation and IκBα degradation, reduced myocardial TNF‐α production and prevented LPS‐provoked cardiac dysfunction. Altogether, these findings indicate that activation of α1‐AR by NE suppresses LPS‐induced cardiomyocyte TNF‐α expression and improves cardiac dysfunction during endotoxaemia via promoting myocardial ERK phosphorylation and suppressing NF‐κB activation. 相似文献
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Christian Starkenmann Fabienne Mayenzet Robert Brauchli Myriam Troccaz 《化学与生物多样性》2013,10(12):2197-2208
5α‐Androst‐16‐en‐3α‐ol (α‐androstenol) is an important contributor to human axilla sweat odor. It is assumed that α‐andostenol is excreted from the apocrine glands via a H2O‐soluble conjugate, and this precursor was formally characterized in this study for the first time in human sweat. The possible H2O‐soluble precursors, sulfate and glucuronide derivatives, were synthesized as analytical standards, i.e., α‐androstenol, β‐androstenol sulfates, 5α‐androsta‐5,16‐dien‐3β‐ol (β‐androstadienol) sulfate, α‐androstenol β‐glucuronide, α‐androstenol α‐glucuronide, β‐androstadienol β‐glucuronide, and α‐androstenol β‐glucuronide furanose. The occurrence of α‐androstenol β‐glucuronide was established by ultra performance liquid chromatography (UPLC)/MS (heated electrospray ionization (HESI)) in negative‐ion mode in pooled human sweat, containing eccrine and apocrine secretions and collected from 25 female and 24 male underarms. Its concentration was of 79 ng/ml in female secretions and 241 ng/ml in male secretions. The release of α‐androstenol was observed after incubation of the sterile human sweat or α‐androstenol β‐glucuronide with a commercial glucuronidase enzyme, the urine‐isolated bacteria Streptococcus agalactiae, and the skin bacteria Staphylococcus warneri DSM 20316, Staphylococcus haemolyticus DSM 20263, and Propionibacterium acnes ATCC 6919, reported to have β‐glucuronidase activities. We demonstrated that if α‐ and β‐androstenols and androstadienol sulfates were present in human sweat, their concentrations would be too low to be considered as potential precursors of malodors; therefore, the H2O‐soluble precursor of α‐androstenol in apocrine secretion should be a β‐glucuronide. 相似文献
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Ann L Cornish Caroline E Sutton Joanne O'Donnell Louise H Cengia Andrew W Roberts Ian P Wicks Kingston H G Mills Ben A Croker 《EMBO reports》2010,11(8):640-646
Reports describing the effect of interferon‐γ (IFNγ) on interleukin‐1β (IL‐1β) production are conflicting. We resolve this controversy by showing that IFNγ potentiates IL‐1β release from human cells, but transiently inhibits the production of IL‐1β from mouse cells. Release from this inhibition is dependent on suppressor of cytokine signalling 1. IL‐1β and Th17 cells are pathogenic in mouse models for autoimmune disease, which use Mycobacterium tuberculosis (MTB), in which IFNγ and IFNβ are anti‐inflammatory. We observed that these cytokines suppress IL‐1β production in response to MTB, resulting in a reduced number of IL‐17‐producing cells. In human cells, IFNγ increased IL‐1β production, and this might explain why IFNγ is detrimental for multiple sclerosis. In mice, IFNγ decreased IL‐1β and subsequently IL‐17, indicating that the adaptive immune response can provide a systemic, but transient, signal to limit inflammation. 相似文献
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Bárbara Lara‐Chacón Mario Bermúdez de León Daniel Leocadio Pablo Gómez Lizeth Fuentes‐Mera Ivette Martínez‐Vieyra Arturo Ortega David A. Jans Bulmaro Cisneros 《Journal of cellular biochemistry》2010,110(3):706-717
β‐dystroglycan (β‐DG) is a widely expressed transmembrane protein that plays important roles in connecting the extracellular matrix to the cytoskeleton, and thereby contributing to plasma membrane integrity and signal transduction. We previously observed nuclear localization of β‐DG in cultured cell lines, implying the existence of a nuclear targeting mechanism that directs it to the nucleus instead of the plasma membrane. In this study, we delineate the nuclear import pathway of β‐DG, characterizing a functional nuclear localization signal (NLS) in the β‐DG cytoplasmic domain, within amino acids 776–782. The NLS either alone or in the context of the whole β‐DG protein was able to target the heterologous GFP protein to the nucleus, with site‐directed mutagenesis indicating that amino acids R779 and K780 are critical for NLS functionality. The nuclear transport molecules Importin (Imp)α and Impβ bound with high affinity to the NLS of β‐DG and were found to be essential for NLS‐dependent nuclear import in an in vitro reconstituted nuclear transport assay; cotransfection experiments confirmed the dependence on Ran for nuclear accumulation. Intriguingly, experiments suggested that tyrosine phosphorylation of β‐DG may result in cytoplasmic retention, with Y892 playing a key role. β‐DG thus follows a conventional Impα/β‐dependent nuclear import pathway, with important implications for its potential function in the nucleus. J. Cell. Biochem. 110: 706–717, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
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Elevated Expression of Hepatoma Up‐Regulated Protein Inhibits γ‐Irradiation‐Induced Apoptosis of Prostate Cancer Cells
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Mohamed Hassan Abdelouahid El Khattouti Ahmed Ejaeidi Tangeng Ma William A. Day Ingrid Espinoza Srinivasan Vijayakumar Christian R. Gomez 《Journal of cellular biochemistry》2016,117(6):1308-1318
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Inhibition of bleomycin‐induced pulmonary fibrosis by bone marrow‐derived mesenchymal stem cells might be mediated by decreasing MMP9, TIMP‐1, INF‐γ and TGF‐β
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Bin Lv Chun‐li Che Da‐ping Fan Li‐feng Wang Yi‐mei Zhang 《Cell biochemistry and function》2015,33(6):356-365
The study was aimed to investigate the mechanism and administration timing of bone marrow‐derived mesenchymal stem cells (BMSCs) in bleomycin (BLM)‐induced pulmonary fibrosis mice. Thirty‐six mice were divided into six groups: control group (saline), model group (intratracheal administration of BLM), day 1, day 3 and day 6 BMSCs treatment groups and hormone group (hydrocortisone after BLM treatment). BMSCs treatment groups received BMSCs at day 1, 3 or 6 following BLM treatment, respectively. Haematoxylin and eosin and Masson staining were conducted to measure lung injury and fibrosis, respectively. Matrix metalloproteinase (MMP9), tissue inhibitor of metalloproteinase‐1 (TIMP‐1), γ‐interferon (INF‐γ) and transforming growth factor β1 (TGF‐β) were detected in both lung tissue and serum. Histologically, the model group had pronounced lung injury, increased inflammatory cells and collagenous fibres and up‐regulated MMP9, TIMP‐1, INF‐γ and TGF‐β compared with control group. The histological appearance of lung inflammation and fibrosis and elevation of these parameters were inhibited in BMSCs treatment groups, among which, day 3 and day 6 treatment groups had less inflammatory cells and collagenous fibres than day 1 treatment group. BMSCs might suppress lung fibrosis and inflammation through down‐regulating MMP9, TIMP‐1, INF‐γ and TGF‐β. Delayed BMSCs treatment might exhibit a better therapeutic effect. Copyright © 2015 John Wiley & Sons, Ltd. Highlights are as follows:
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Yiyi Hu Xi Chen Huiqin Duan Yuanliang Hu Xiang Mu 《Cell biochemistry and function》2009,27(5):284-288
To investigate the pharmacological mechanism of the traditional Chinese medicine, Pulsatilla decoction (PD), the levels of nitric oxide (NO), endothelin‐1 (ET‐1), tumor necrosis factor‐α (TNF‐α), and interleukin‐1α (IL‐1α) secreted by cultured rat intestinal microvascular endothelial cells (RIMECs) were determined after treatment with PD and its seven active ingredients, namely anemoside B4, anemonin, berberine, jatrorrhizine, palmatine, aesculin, and esculetin. RIMECs were challenged with lipopolysaccharide (LPS) at 1 µg ml?1 for 3 h and then treated with PD at 1, 5, and 10 mg ml?1 and its seven ingredients at 1, 5, and 10 µg ml?1 for 21 h, respectively. The results revealed that PD, anemonin, berberine, and esculetin inhibited the production of NO; PD, anemonin, and esculetin inhibited the secretion of ET‐1; PD, anemoside B4, berberine, jatrorrhizine, and aesculin downregulated TNF‐α expression; PD, anemoside B4, berberine, and palmatine decreased the content of IL‐1α. It showed that PD and its active ingredients could significantly inhibit the secretion of NO, ET‐1, TNF‐α, and IL‐1α in LPS‐induced RIMECs and suggested they would reduce inflammatory response via these cytokines. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献
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LIPUS suppressed LPS‐induced IL‐1α through the inhibition of NF‐κB nuclear translocation via AT1‐PLCβ pathway in MC3T3‐E1 cells
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Mayu Nagao Natsuko Tanabe Soichiro Manaka Masako Naito Jumpei Sekino Tadahiro Takayama Takayuki Kawato Go Torigoe Shunichiro Kato Naoya Tsukune Masao Maeno Naoto Suzuki Shuichi Sato 《Journal of cellular physiology》2017,232(12):3337-3346
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SIRT1 expression is refractory to hypoxia and inflammatory cytokines in nucleus pulposus cells: Novel regulation by HIF‐1α and NF‐κB signaling
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Xiaofei Wang Hongjian Li Kang Xu Haipeng Zhu Yan Peng Anjing Liang Chunhai Li Dongsheng Huang Wei Ye 《Cell biology international》2016,40(6):716-726
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The family of 14‐3‐3 proteins and specifically 14‐3‐3σ are up‐regulated during the development of renal pathologies
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Myrto Rizou Eleni A. Frangou Filio Marineli Niki Prakoura Jerome Zoidakis Harikleia Gakiopoulou George Liapis Panagiotis Kavvadas Christos Chatziantoniou Manousos Makridakis Antonia Vlahou John Boletis Demetrios Vlahakos Dimitrios Goumenos Evgenios Daphnis Christos Iatrou Aristidis S. Charonis 《Journal of cellular and molecular medicine》2018,22(9):4139-4149
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Ci‐You Huang Wei‐Feng Yao Wei‐guo Wu Yu‐Lian Lu Hui Wan Wen Wang 《Cell biochemistry and function》2013,31(6):468-475
Tumour necrosis factor‐α (TNF‐ α)is a major contributor to the pathogenesis of insulin resistance associated with obesity and type 2 diabetes. It has been found that endogenous hydrogen sulfide (H2S) contributes to the pathogenesis of diabetes. We have hypothesized that TNF‐α‐induced insulin resistance is involved in endogenous H2S generation. The aim of the present study is to investigate the role of endogenous H2S in TNF‐α‐induced insulin resistance by studying 3T3‐L1 adipocytes. We found that treatment of 3T3‐L1 adipocytes with TNF‐α leads to deficiency in insulin‐stimulated glucose consumption and uptake and increase in endogenous H2S generation. We show that cystathionine γ‐lyase (CSE) is catalysed in 3T3‐L1 adipocytes to generate H2S and that CSE expression and activity are upregulated by TNF‐α treatment. Inhibited CSE by its potent inhibitors significantly attenuates TNF‐α‐induced insulin resistance in 3T3‐L1 adipocytes, whereas H2S treatment of 3T3‐L1 adipocytes impairs insulin‐stimulated glucose consumption and uptake. These data indicate that endogenous CSE/H2S system contributes to TNF‐α‐caused insulin resistance in 3T3‐L1 adipocytes. Our findings suggest that modulation of CSE/H2S system is a potential therapeutic avenue for insulin resistance. Copyright © 2012 John Wiley & Sons, Ltd. 相似文献