scholarly journals Sulforaphane induces Nrf2 target genes and attenuates inflammatory gene expression in microglia from brain of young adult and aged mice

2016 ◽  
Vol 73 ◽  
pp. 42-48 ◽  
Author(s):  
Brigitte E. Townsend ◽  
Rodney W. Johnson
Keyword(s):  
Gene Expression ◽  
Young Adult ◽  
Target Genes ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Aged Mice

scholarly journals IκBα is required for full transcriptional induction of some NFκB-regulated genes in response to TNF in MCF-7 cells

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Minami Ando ◽  
Shigeyuki Magi ◽  
Masahide Seki ◽  
Yutaka Suzuki ◽  
Takeya Kasukawa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Negative Feedback ◽  
Target Genes ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Transcriptional Induction ◽  
Feedback Regulator ◽  
Mcf 7 ◽  
Transcription Cycle

AbstractInflammatory stimuli triggers the degradation of three inhibitory κB (IκB) proteins, allowing for nuclear translocation of nuclear factor-κB (NFκB) for transcriptional induction of its target genes. Of these three, IκBα is a well-known negative feedback regulator that limits the duration of NFκB activity. We sought to determine whether IκBα’s role in enabling or limiting NFκB activation is important for tumor necrosis factor (TNF)-induced gene expression in human breast cancer cells (MCF-7). Contrary to our expectations, many more TNF-response genes showed reduced induction than enhanced induction in IκBα knockdown cells. Mathematical modeling was used to investigate the underlying mechanism. We found that the reduced activation of some NFκB target genes in IκBα-deficient cells could be explained by the incoherent feedforward loop (IFFL) model. In addition, for a subset of genes, prolonged NFκB activity due to loss of negative feedback control did not prolong their transient activation; this implied a multi-state transcription cycle control of gene induction. Genes encoding key inflammation-related transcription factors, such as JUNB and KLF10, were found to be best represented by a model that contained both the IFFL and the transcription cycle motif. Our analysis sheds light on the regulatory strategies that safeguard inflammatory gene expression from overproduction and repositions the function of IκBα not only as a negative feedback regulator of NFκB but also as an enabler of NFκB-regulated stimulus-responsive inflammatory gene expression. This study indicates the complex involvement of IκBα in the inflammatory response to TNF that is induced by radiation therapy in breast cancer.

Dysregulation of inflammatory gene expression in lesional and nonlesional skin of patients with pyoderma gangrenosum

2017 ◽  
Vol 178 (1) ◽  
Author(s):  
A.G. Ortega‐Loayza ◽  
W.H. Nugent ◽  
O.M. Lucero ◽  
S.L. Washington ◽  
J.R. Nunley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pyoderma Gangrenosum ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Gene Expression Profile in Delay Graft Function: Inflammatory Markers Are Associated with Recipient and Donor Risk Factors

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Diego Guerrieri ◽  
Luis Re ◽  
Jorgelina Petroni ◽  
Nella Ambrosi ◽  
Roxana E. Pilotti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Risk Factors ◽  
Kidney Transplantation ◽  
Inflammatory Markers ◽  
Graft Function ◽  
Deceased Donor ◽  
Specific Pattern ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Recipient Age

Background.Delayed graft function (DGF) remains an important problem after kidney transplantation and reduced long-term graft survival of the transplanted organ. The aim of the present study was to determine if the development of DGF was associated with a specific pattern of inflammatory gene expression in expanded criteria of deceased donor kidney transplantation. Also, we explored the presence of correlations between DGF risk factors and the profile that was found.Methods.Seven days after kidney transplant, a cDNA microarray was performed on biopsies of graft from patients with and without DGF. Data was confirmed by real-time PCR. Correlations were performed between inflammatory gene expression and clinical risk factors.Results.From a total of 84 genes analyzed, 58 genes were upregulated while only 1 gene was downregulated in patients with DGF compared with no DGF (P=0.01). The most relevant genes fold changes observed was IFNA1, IL-10, IL-1F7, IL-1R1, HMOX-1, and TGF-β. The results were confirmed for IFNA1, IL-1R1, HMOX-1 and TGF-β. A correlation was observed between TGF-β, donor age, and preablation creatinine, but not body mass index (BMI). Also, TGF-βshowed an association with recipient age, while IFNA1 correlated with recipient BMI. Furthermore, TGF-β, IFNA1 and HMOX-1 correlated with several posttransplant kidney function markers, such as diuresis, ultrasound Doppler, and glycemia.Conclusions.Overall, the present study shows that DGF is associated with inflammatory markers, which are correlated with donor and recipient DGF risk factors.

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