Gene Expression Analysis of Innate Immune Compromised Mice Reveals Secondary Target Genes in Response to Intracortical Microelectrode Implantation

2021 ◽  
Author(s):  
Sydney Song ◽  
Hillary W. Bedell ◽  
Brianna J. Regan ◽  
Evon S. Ereifej ◽  
Ricky Chan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Innate Immune ◽  
Secondary Target

scholarly journals Gene expression analysis of the innate immune system during early rearing and weaning of meagre (Argyrosomus regius)

2019 ◽  
Vol 94 ◽  
pp. 819-832
Author(s):  
Cindy Campoverde ◽  
Douglas J. Milne ◽  
Christopher J. Secombes ◽  
Alicia Estévez ◽  
Enric Gisbert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Expression Analysis ◽  
Innate Immune System ◽  
Gene Expression Analysis ◽  
Innate Immune ◽  
Argyrosomus Regius ◽  
Early Rearing

Comparative Cytological and Gene Expression Analysis Reveals Potential Metabolic Pathways and Target Genes Responsive to Salt Stress in Kenaf (Hibiscus cannabinus L.)

2020 ◽  
Vol 39 (3) ◽  
pp. 1245-1260 ◽  
Author(s):  
Muhammad Haneef Kashif ◽  
Danfeng Tang ◽  
Zengqiang Li ◽  
Fan Wei ◽  
Zhichen Liang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Salt Stress ◽  
Expression Analysis ◽  
Metabolic Pathways ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Hibiscus Cannabinus

Global Gene Expression Analysis Demonstrates that Transforming Growth Factor β1 (TGF-β1) Signals Exclusively through Receptor Complexes Involving TGF-β Receptor I and Identifies Numerous Targets of TGF-β Signaling.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2178-2178
Author(s):  
Goran Karlsson ◽  
Yingchun Liu ◽  
Marie-José Goumans ◽  
Jonas Larsson ◽  
Ju-Seog Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Global Gene Expression ◽  
Differentially Expressed ◽  
Global Gene Expression Analysis ◽  
Β Receptor ◽  
Tgf Β1

Abstract In the hematopoietic system, TGF-β1 is one of the most potent extrinsic regulators, affecting both early progenitors and committed cells. At the top of the hematopoietic hierarchy, TGF-β1 maintains hematopoietic stem cells (HSCs) in quiescence in vitro through transcriptional regulation of genes encoding proteins important in the cell cycle. We have shown that TGF-β receptor I (TβRI) −/− HSCs exhibit increased proliferative capacity in vitro and that TβRII−/− mice develop a multifocal autoimmune disease, mainly mediated by T-cells (Larsson et al, 2003, Levéen et al 2002). The mechanisms of TGF-β signaling in hematopoietic cells are poorly understood and many target genes of TGF-β signaling remain elusive. In this study we have used global gene expression analysis to investigate whether all TGF-β signaling is mediated by TβRI and II. Furthermore, we asked what target genes are affected upon TGF-β stimulation in normal and TGF-β signaling deficient murine embryonic fibroblasts (MEFs). MEFs were grown with and without TGF-β1 stimulation and proliferation, transcriptional responses and expression analysis were performed. We demonstrate through Western Blot analysis, luciferase reporter assays and cell expansion experiments how these cells lack functional TβRI. Additionally, transcriptional assays show that no other Smad activity is triggered by TGF-β1 stimulation. Furthermore, we demonstrate through quantitative RT-PCR that the inhibitor of differentiation family of genes, known targets of TGF-β signaling, are not affected by TGF-β1 in TβRI−/− MEFs, while wt cells downregulate these genes 4–8.5 fold in response to stimulation. In order to completely exclude alternative receptors outside the TGF-β superfamily and signaling pathways activated through TβRII alone, we performed global gene expression profiling on TGF-β1 stimulated TβRI−/− MEFs with unstimulated TβRI deficient cells as reference. Very few (0.05 %) of the more than 37,000 spots on the microarray had a >2 fold differential expression in the two experiments conducted. Similar experiments performed on wt cells resulted in differential expression of between 2.6–3.9 % of the genes printed. From this data we conclude that no signaling affecting gene expression occur in the absence of TβRI in these cells. Additionally we present transcriptional profiles of MEF cell lines that either are normal or are TβRI deficient. By means of cDNA microarray technology, we have identified genes that were differentially expressed when TβRI deficient fibroblasts were compared to wt cells stimulated with TGF-β1. Our results create a data base of 461 significantly differentially expressed (p<0.01) target genes of TGF-β signaling. These include genes potentially responsible for the growth arrest induced by TGF-β1, like Gadd45g, Gas5, Id1, Id2 and Id3. However, the most significantly enriched number of differentially expressed genes are involved in protein folding and chaperone activities (Hspa9a, Hsp105, Hspe1, Hsp60, Cct2, Cct3, Cct8, Tcp1 and Dnaja1. Studies to identify TGF-β signaling responsive genes in HSCs are in progress.

Global gene expression analysis on the target genes of PQS and HHQ in J774A.1 monocyte/macrophage cells

2010 ◽  
Vol 49 (4) ◽  
pp. 174-180 ◽  
Author(s):  
Kiwan Kim ◽  
Seol-Hee Kim ◽  
Francois Lépine ◽  
You-Hee Cho ◽  
Gap Ryol Lee
Keyword(s):  
Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Global Gene Expression ◽  
Macrophage Cells ◽  
Global Gene Expression Analysis

Corrigendum to “Gene expression analysis during dengue virus infection in HepG2 cells reveals virus control of innate immune response” [Journal of Infection 2010;60:65–75]

2010 ◽  
Vol 61 (4) ◽  
pp. 360
Author(s):  
Thaís M. Conceição ◽  
Tatiana El-Bacha ◽  
Camila S.A. Villas-Bôas ◽  
Gerardo Coello ◽  
Jorge Ramírez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Virus Infection ◽  
Dengue Virus ◽  
Innate Immune Response ◽  
Expression Analysis ◽  
Hepg2 Cells ◽  
Gene Expression Analysis ◽  
Innate Immune ◽  
Dengue Virus Infection

Gene-expression analysis identifies novel RBL2/p130 target genes in endemic Burkitt lymphoma cell lines and primary tumors

Blood ◽  
2007 ◽  
Vol 110 (4) ◽  
pp. 1301-1307 ◽  
Author(s):  
Giulia De Falco ◽  
Eleonora Leucci ◽  
Dido Lenze ◽  
Pier Paolo Piccaluga ◽  
Pier Paolo Claudio ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Growth ◽  
Cell Lines ◽  
Expression Analysis ◽  
Burkitt Lymphoma ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Growth Control ◽  
Primary Tumors ◽  
Cell Growth And Viability

Abstract Burkitt lymphoma (BL) is a B-cell tumor whose characteristic gene aberration is the translocation t(8;14), which determines c-myc overexpression. Several genetic and epigenetic alterations other than c-myc overexpression have also been described in BL. It has been demonstrated that the RBL2/p130 gene, a member of the retinoblastoma family (pRbs), is mutated in BL cell lines and primary tumors. The aim of this study was to investigate the biologic effect of RBL2/p130 in BL cells and its possible role in lymphomagenesis. Therefore, we reintroduced a functional RBL2/p130 in BL cell lines where this gene was mutated. Our results demonstrated that RBL2/p130-transfected cells regain growth control. This suggests that RBL2/p130 may control the expression of several genes, which may be important for cell growth and viability. Gene-expression analysis revealed a modulation of several genes, including CGRRF1, RGS1, BTG1, TIA1, and PCDHA2, upon RBL2/p130 reintroduction. We then monitored their expression in primary tumors of endemic BL as well, demonstrating that their expression resembled those of the BL cell lines. In conclusion, these data suggest that, as RBL2/p130 modulates the expression of target genes, which are important for cell growth and viability, its inactivation may be relevant for the occurrence of BL.

Gene expression analysis during recovery process indicates the mechanism for innate immune injury and repair from Coxsackievirus B3-induced myocarditis

2016 ◽  
Vol 213 ◽  
pp. 314-321 ◽  
Author(s):  
Hai-Lan Yao ◽  
Juan Song ◽  
Peng Sun ◽  
Qin-Qin Song ◽  
Lin-Jun Sheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Recovery Process ◽  
Coxsackievirus B3 ◽  
Innate Immune ◽  
Immune Injury ◽  
Injury And Repair

NFAT2 Regulates Anergy Induction in CLL through Lck

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 720-720
Author(s):  
Melanie Märklin ◽  
Jonas S. Heitmann ◽  
Alexandra Poljak ◽  
Stefanie Bugl ◽  
Hans-Georg Kopp ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
B Cell ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Target Genes ◽  
Cell Phenotype ◽  
Resting Cells ◽  
Aggressive Disease

Abstract NFAT is a family of highly phosphorylated proteins residing in the cytoplasm of resting cells. Upon dephosphorylation by calcineurin, NFAT proteins translocate to the nucleus where they orchestrate developmental and activation programs in diverse cell types. CLL is a clonal disorder of mature B cells characterized by the expression of CD19, CD23 and CD5. With respect to prognosis, it constitutes a heterogeneous disease with some patients exhibiting an indolent course for many years and others progressing rapidly and requiring early treatment. A defined subgroup of patients shows enhanced responsiveness to stimulation of the B cell receptor (BCR) complex and more aggressive disease. In contrast, another subset of CLL patients with more indolent course is characterized by an anergic B cell phenotype referring to B cell unresponsiveness to IgM ligation and essential lack of phosphotyrosine induction and calcium flux. Here, we analyzed the role of NFAT2 in the pathogenesis of B-CLL and in anergy induction in CLL cells. For this purpose, we generated conditional CD19-Cre NFAT2 knock out mice, which exhibit NFAT2 deletion limited to the B cell lineage. To investigate the role of NFAT2 in the pathogenesis of CLL, we used the Eµ-TCL1 transgenic mouse model. TCL1 transgenic mice develop a human-like CLL at the age of approximately 14 weeks to which the animals eventually succumb at an average age of 10 months. We generated TCL1+NFAT2 ko mice with TCL1 transgenic mice without an NFAT2 deletion serving as controls. To identify novel NFAT2 target genes in CLL cells, we also performed a comparative gene expression analysis on CLL cells with intact NFAT2 expression and on CLL cells with NFAT2 deletion using affymetrix microarrays. In order to asses the anergic phenotype in CLL cells and the role of NFAT2 in its induction, we performed Ca2+ mobilization assays using a flow cytometric approach and performed Western Blots for multiple downstream signaling molecules. Mice with NFAT2 ko exhibited a significantly more aggressive disease course with accelerated accumulation of CD5+CD19+ CLL cells in different organs, significantly higher proliferation rates and a dramatically reduced life expectancy (200 vs. 325 days) as compared to TCL1 control animals. To identify NFAT2 target genes responsible for the observed alterations in the disease phenotype, we subsequently performed a gene expression analysis with CLL cells from both leukemic cohorts. Here, we detected a substantially altered expression profile of genes associated with B cell anergy in the TCL1+NFAT2 ko mice. The vast majority of these genes was expressed significantly less in the absence of NFAT2 with Lck, Pacsin1 and the E3 ligase Cbl representing the biggest hits. To further delineate the anergic phenotype and the role of NFAT2 in its induction, we subsequently performed Ca2+ mobilization assays. While anergic CLL cells from TCL1 mice exhibited an unresponsive phenotype with respect to Ca2+ flux upon IgM ligation, TCL1+NFAT2 ko mice showed an entirely normal capacity to mobilize intracellular Ca2+. Furthermore, IgM stimulation did not activate normal phosphotyrosine induction (phosphorylation of AKT and ERK kinases) in TCL1 mice while NAFT2-deficient CLL cells exhibited an unremarkable activation pattern with respect to AKT and ERK as assessed by Western Blotting. NFAT2-deficient CLL cells on the contrary exhibited compromised activation of the anergy regulator Lck as assessed by Y394 phosphorylation. Bypassing the BCR by antigen-independent stimulation with CD40 and LPS demonstrated slightly increased proliferation in anergic TCL1 CLL cells while NFAT2-deficient CLL cells exhibited massive proliferation. In summary, our data provide strong evidence that genetic loss of NFAT2 leads to more aggressive disease in CLL which is associated with the loss of the anergic phenotype. We could show that NFAT2 controls the expression of several important anergy-associated genes and identified Lck as a critical target of NFAT2 in this context. Taken together, our data demonstrate that the NFAT2-Lck axis plays an essential role in the pathogenesis of CLL and implicate it as a potential target in its treatment. Disclosures No relevant conflicts of interest to declare.

Sign in / Sign up

Export Citation Format

Share Document