Modulation of NF-κB–Dependent Gene Expression by H2O2: A Major Role for a Simple Chemical Process in a Complex Biological Response

2009 ◽  
Vol 11 (9) ◽  
pp. 2043-2053 ◽  
Author(s):  
Virgínia Oliveira-Marques ◽  
H. Susana Marinho ◽  
Luísa Cyrne ◽  
Fernando Antunes
2017 ◽  
Vol 53 (76) ◽  
pp. 10548-10551 ◽  
Author(s):  
Deliang Zhang ◽  
Bin-Bin Cui ◽  
Chenxiao Zhou ◽  
Liang Li ◽  
Yihua Chen ◽  
...  

A simple chemical process was developed in a scalable manner, to reduce trap states in perovskite absorbers from the very beginning.


2011 ◽  
Vol 392 (12) ◽  
pp. 1123-1134 ◽  
Author(s):  
Christina Khouri ◽  
Anna Dittrich ◽  
Sara Dutton Sackett ◽  
Bernd Denecke ◽  
Christian Trautwein ◽  
...  

AbstractInflammation is the biological response to injurious stimuli. In the initial phase of the inflammatory process, interleukin-6 (IL-6) is the main inducer of acute phase protein expression in the liver. A prolonged acute phase response is characterised by a disturbed glucose homeostasis and elevated levels of IL-6, insulin, and counterregulatory hormones such as glucagon. Several studies deal with the impact of IL-6 on glucagon-dependent gene expression. In contrast, only very little is known about the influence of G-protein-coupled receptors on IL-6 signalling. Therefore, the aim of this study is to elucidate the regulation of IL-6-induced gene expression by glucagon. We could reveal a novel mechanism of negative regulation of IL-6-induced MAP kinase activation by glucagon in primary murine hepatocytes. IL-6-dependent induction of the ERK-dependent target geneTfpi2, coding for a Kunitz-type serine protease inhibitor, was strongly down-regulated by glucagon treatment. Studying the underlying mechanism revealed a redundant action of the signalling molecules exchange protein activated by cyclic AMP (Epac) and protein kinase A. The metabolic hormone glucagon interferes in IL-6-induced gene expression. This observation is indicative for a regulatory role of G-protein-coupled receptors in the IL-6-dependent inflammatory response.


2018 ◽  
Vol 47 (13) ◽  
pp. 4501-4507 ◽  
Author(s):  
A. Sett ◽  
D. Das ◽  
D. Banerjee ◽  
U. K. Ghorai ◽  
N. S. Das ◽  
...  

Zinc oxide (ZnO) nanorods (NRs) wrapped with graphitic carbon nitride (GCN) nanosheet (NS) hybrids have been synthesized by a simple chemical process.


2020 ◽  
Author(s):  
A. Rowan-Carroll ◽  
A. Reardon ◽  
K. Leingartner ◽  
R. Gagné ◽  
A. Williams ◽  
...  

AbstractPer- and poly-fluoroalkyl substances (PFAS) are widely found in the environment because of their extensive use and persistence. Although a few PFAS are well studied, most lack toxicity data to inform human health hazard and risk assessment. This study focussed on four model PFAS: perfluorooctanoic acid (PFOA; 8 carbon), perfluorobutane sulfonate (PFBS; 4 carbon), perfluorooctane sulfonate (PFOS; 8 carbon), and perfluorodecane sulfonate (PFDS; 10 carbon). Human primary liver cell spheroids (i.e., pooled-donor) were exposed to 10 concentrations of PFAS over four time-points. The approach aimed to: (1) identify the extent to which the PFAS modulated gene expression; (2) identify similarities in biological responses; (3) compare PFAS potency through benchmark concentration (BMC) analysis; and (4) derive bioactivity exposure ratios (BERs: ratio of concentration at which biological response occurs converted to administered equivalent dose relative to human daily exposure). All PFAS induced transcriptional changes of cholesterol biosynthesis and lipid metabolism, and appeared to activate PPARα. PFOS exhibited the most transcriptional perturbations and had a highly similar gene expression profile to PFDS. PFBS induced the least transcriptional changes and had the highest BMCs. The data indicate that these four chemicals may have common molecular targets and toxicities, but that PFOS and PFDS are the most similar. BERs derived for PFOA and PFOS had relatively low margins; the transcriptomic BER was slightly more conservative than BERs derived from rodent apical endpoints used as points of departure in risk assessment. The data provide a baseline on which to compare the toxicity of other PFAS using this testing strategy.


2007 ◽  
Vol 102 (1) ◽  
pp. 42-60 ◽  
Author(s):  
Sharon E. Hook ◽  
Ann D. Skillman ◽  
Banu Gopalan ◽  
Jack A. Small ◽  
Irvin R. Schultz

2008 ◽  
Vol 8 (6) ◽  
pp. 552-560 ◽  
Author(s):  
Daniel Haschtmann ◽  
Stephen J. Ferguson ◽  
Jivko V. Stoyanov

Object The object of this study was to characterize the biological response of isolated intervertebral disc fragments to in vitro culture conditions with respect to cell death and inflammatory and catabolic changes. The acquired data could help to gain a better understanding of the biological reaction of disc tissue when exposed to environmental changes along with altered nutritional and osmotic conditions, as are encountered in different in vitro disc models or disc diseases in vivo. Methods Intervertebral disc anulus fragments were isolated from Burgundy rabbits and cultured in standard media for 3 days. The disc fragments were analyzed for their swelling properties, proteoglycan loss on histological studies, lactate dehydrogenase activity, apoptosis, gene expression of collagenases and gelatinases, and for proinflammatory (MCP-1, IL-8, and IL-6) and apoptosis-associated (TNF-α, Fas-L, and caspase 3) genes. Results The results demonstrate that disc specimens were swelling, and a loss of proteoglycans with disarrangement of anulus architecture was observed. The disc cells underwent rapid apoptosis with upregulation of various proinflammatory genes. Both collagenases, matrix metalloproteinase (MMP)–1 and MMP-13, were increasingly transcribed, whereas the gelatinases MMP-2 and MMP-9 did not respond or were downregulated. Conclusions Cultured disc fragments swell and undergo necrotic and apoptotic cell death combined with a catabolic gene response and gene expression of proinflammatory and chemoattractant proteins. Some of these findings have been demonstrated before in various spinal disorders. In addition, disc fragments are not suitable for long-term culture if a stable disc metabolism is desired, and the described changes have to be considered when using isolated disc material for in vitro cultures.


2012 ◽  
Vol 5 (11 Supplement) ◽  
pp. B07-B07
Author(s):  
Kahkeshan Hijazi ◽  
Bozena Malyszko ◽  
Xiaohui Zhang ◽  
Gang Liu ◽  
Yuriy Alekseyev ◽  
...  

2004 ◽  
Vol 286 (2) ◽  
pp. C355-C364 ◽  
Author(s):  
Ilona A. Barash ◽  
Liby Mathew ◽  
Allen F. Ryan ◽  
Ju Chen ◽  
Richard L. Lieber

Eccentric contractions (ECs), in which a muscle is forced to lengthen while activated, result in muscle injury and, eventually, muscle strengthening and prevention of further injury. Although the mechanical basis of EC-induced injury has been studied in detail, the biological response of muscle is less well characterized. This study presents the development of a minimally invasive model of EC injury in the mouse, follows the time course of torque recovery after an injurious bout of ECs, and uses Affymetrix microarrays to compare the gene expression profile 48 h after ECs to both isometrically stimulated muscles and contralateral muscles. Torque dropped by ∼55% immediately after the exercise bout and recovered to initial levels 7 days later. Thirty-six known genes were upregulated after ECs compared with contralateral and isometrically stimulated muscles, including five muscle-specific genes: muscle LIM protein (MLP), muscle ankyrin repeat proteins (MARP1 and -2; also known as cardiac ankyrin repeat protein and Arpp/Ankrd2, respectively), Xin, and myosin binding protein H. The time courses of MLP and MARP expression after the injury bout (determined by quantitative real-time polymerase chain reaction) indicate that these genes are rapidly induced, reaching a peak expression level of 6–11 times contralateral values 12–24 h after the EC bout and returning to baseline within 72 h. Very little gene induction was seen after either isometric activation or passive stretch, indicating that the MLP and MARP genes may play an important and specific role in the biological response of muscle to EC-induced injury.


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