Quantifying Microbially Mediated Kinetics of Ferrihydrite Transformation and Arsenic Reduction: Role of the Arsenate-Reducing Gene Expression Pattern

2020 ◽  
Vol 54 (11) ◽  
pp. 6621-6631 ◽  
Author(s):  
Zhenqing Shi ◽  
Shiwen Hu ◽  
Jingyi Lin ◽  
Tongxu Liu ◽  
Xiaomin Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Arsenic Reduction ◽  
Kinetics Of

scholarly journals Stress signaling and STAT1 activation characterize the keratinocytic gene expression pattern in Hidradenitis suppurativa

2021 ◽  
Author(s):  
VG Frings ◽  
L Jopp ◽  
M Srivastava ◽  
D Presser ◽  
M Goebeler ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
Rna Sequencing ◽  
Expression Pattern ◽  
Hidradenitis Suppurativa ◽  
Gene Expression Pattern ◽  
Epidermal Keratinocytes ◽  
Stress Signaling ◽  
Promising Therapeutic Approach

ABSTRACTBackgroundThe underlying pathogenetic factors generating the innate immune signal necessary for T cell activation, initiation and chronification of Hidradenitis suppurativa (HS, also known as Acne inversa) are still poorly understood. Emerging evidence suggests that defective keratinocyte function critically contributes to HS disease development and progression.ObjectivesTo elucidate the role of keratinocytes in HS lesion formation, we compared the transcriptomes of isolated lesional and perilesional HS epidermis by RNA sequencing.MethodsLesional and perilesional HS skin samples of at least 3 different donors were obtained. Isolated epidermal keratinocytes were further processed for cell culture, protein extraction, immunostaining procedures or RNA isolation and RNA sequencing. For large scale promotor site analysis, DEGs were analyzed for overrepresented transcription factor binding sites. Functional annotation clustering for analyzing enriched functional-related gene groups was performed employing the DAVID Bioinformatics Resources.ResultsWe show that HS is characterized by a strong epidermal stress state as evident by a significant overrepresentation of an AP-1-driven stress signature in the overall gene expression pattern of lesional keratinocytes and a substantial activation of the stress-activated cJun N-terminal kinase (JNK) pathway in lesional HS epidermis. Additionally, our data reveal a strong induction of STAT1 activation in lesional HS epidermis that likely results from IFNγ production and governs the expression of key inflammatory genes that coordinate activation of innate immunity and the adaptive T cell response in HS.ConclusionsTaken together, these data implicate a new role of combined stress signaling and JAK/STAT1 pathway activation in disease progression of HS suggesting interference with JAK/STAT1 signaling as a potentially promising therapeutic approach for HS.

scholarly journals Gene expression profiling identifies FLT3 mutation-like cases in wild-type FLT3 acute myeloid leukemia

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247093
Author(s):  
Adrián Mosquera Orgueira ◽  
Andrés Peleteiro Raíndo ◽  
Miguel Cid López ◽  
Beatriz Antelo Rodríguez ◽  
José Ángel Díaz Arias ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Wild Type ◽  
Wilcoxon Rank Sum Test ◽  
Recurrent Mutations ◽  
Flt3 Inhibitors ◽  
Predictive Role ◽  
Acute Myeloid

Background FLT3 mutation is present in 25–30% of all acute myeloid leukemias (AML), and it is associated with adverse outcome. FLT3 inhibitors have shown improved survival results in AML both as upfront treatment and in relapsed/refractory disease. Curiously, a variable proportion of wild-type FLT3 patients also responded to these drugs. Methods We analyzed 6 different transcriptomic datasets of AML cases. Differential expression between mutated and wild-type FLT3 AMLs was performed with the Wilcoxon-rank sum test. Hierarchical clustering was used to identify FLT3-mutation like AMLs. Finally, enrichment in recurrent mutations was performed with the Fisher’s test. Results A FLT3 mutation-like gene expression pattern was identified among wild-type FLT3 AMLs. This pattern was highly enriched in NPM1 and DNMT3A mutants, and particularly in combined NPM1/DNMT3A mutants. Conclusions We identified a FLT3 mutation-like gene expression pattern in AML which was highly enriched in NPM1 and DNMT3A mutations. Future analysis about the predictive role of this biomarker among wild-type FLT3 patients treated with FLT3 inhibitors is envisaged.

scholarly journals Sphingolipid Metabolic Pathway: An Overview of Major Roles Played in Human Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Raghavendra Pralhada Rao ◽  
Nanditha Vaidyanathan ◽  
Mathiyazhagan Rengasamy ◽  
Anup Mammen Oommen ◽  
Neeti Somaiya ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Expression Pattern ◽  
Metabolic Pathway ◽  
Membrane Lipids ◽  
Gene Expression Pattern ◽  
Bioactive Molecules ◽  
Cellular Processes ◽  
Key Players

Sphingolipids, a family of membrane lipids, are bioactive molecules that participate in diverse functions controlling fundamental cellular processes such as cell division, differentiation, and cell death. Given that most of these cellular processes form the basis for several pathologies, it is not surprising that sphingolipids are key players in several pathological processes. This review discusses the role of the sphingolipid metabolic pathway in diabetes, Alzheimer’s disease, and hepatocellular carcinoma, with a special emphasis on the changes in gene expression pattern in these disease conditions. For convenience, the sphingolipid metabolic pathway is divided into hypothetical compartments (modules) with each compartment representing a physiological process and changes in gene expression pattern are mapped to each of these modules. It appears that alterations in the gene expression pattern in these disease conditions are biased to manipulate the system in order to result in a particular disease.

Abstract 14620: LncExACT1 Acts as a Pivotal Switch Between Physiological and Pathological Cardiac Growth

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Haobo Li ◽  
Lena E Trager ◽  
Xiaojun Liu ◽  
Margaret H Hastings ◽  
CHUNYANG XIAO ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Cardiac Development ◽  
Wheel Running ◽  
Gene Expression Pattern ◽  
Beneficial Effects ◽  
Pathological Hypertrophy ◽  
Physiological Hypertrophy ◽  
Fractional Shortening

Rationale: Pathological hypertrophy commonly leads to heart failure (HF) and loss of cardiomyocytes, while physiological hypertrophy protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain unclear. While long noncoding RNAs (lncRNAs) are important in cardiac development and disease, their role in physiological hypertrophy is unknown. Objective: To investigate the role of lncRNAs in physiological hypertrophy. Methods and Results: Mice underwent voluntary wheel running for eight weeks or transverse aortic constriction (TAC) for two or ten weeks. RNAseq identified a novel set of lncRNAs altered in exercised hearts, which we termed l ong n on c oding Ex ercise- A ssociated C ardiac T ranscripts (lncExACTs). lncExACT1 was highly conserved and uniquely downregulated in exercised hearts but upregulated in pathological animal models and hearts from HF patients vs controls (1.8-fold; p <0.001, N=24) as well as plasma from HF patients with reduced (2.9-fold; p =0.032, N=16) and preserved ejection fraction (3.4-fold; p =0.006, N=18). In mice, AAV9 lncExACT1 overexpression increased cardiac lncExACT1 7-fold at 16 weeks and increased heart (HW) and lung (LW) weight relative to tibial length (TL), reduced fractional shortening (FS) and increased relative wall thickness (RWT) ( p <0.05 for all). These changes were associated with a pathological gene expression pattern. In contrast, antisense lncExACT1 inhibition reduced cardiac expression 2-fold at 2 weeks and increased HW/TL without an increase in LW/TL, improved cardiac function, and increased RWT ( p <0.05 for all). LncExACT1 inhibition induced a physiological gene expression pattern and increased markers of cardiomyogenesis. LncExACT1 inhibition reduced TAC-induced HW/TL and fibrosis, while increasing FS ( p <0.05 for all). Mechanistic studies revealed that lncExACT1 works by binding miR-222 and as a novel regulator of Hippo/Yap1 signaling through modulation of dachsous cadherin-related 2. Conclusions: lncExACT1 acts as a master switch toggling the heart between physiological and pathological growth and provides a potentially tractable therapeutic target for harnessing the beneficial effects of exercise.

Extracellular matrix composition significantly influences pancreatic stellate cell gene expression pattern: role of transgelin in PSC function

2013 ◽  
Vol 305 (6) ◽  
pp. G408-G417 ◽  
Author(s):  
Minoti V. Apte ◽  
Lu Yang ◽  
Phoebe A. Phillips ◽  
Zhihong Xu ◽  
Warren Kaplan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Pancreatitis ◽  
Expression Pattern ◽  
Gene Array ◽  
Gene Expression Pattern ◽  
Collagen I ◽  
Pancreatic Stellate Cells ◽  
Matrix Composition ◽  
Actin Stress Fiber

Activated pancreatic stellate cells (PSCs) are responsible for the fibrotic matrix of chronic pancreatitis and pancreatic cancer. In vitro protocols examining PSC biology have usually involved PSCs cultured on plastic, a nonphysiological surface. However, PSCs cultured on physiological matrices, e.g., Matrigel (normal basement membrane) and collagen (fibrotic pancreas), may have distinctly different behaviors compared with cells cultured on plastic. Therefore, we aimed to 1) compare PSC gene expression after culture on plastic, Matrigel, and collagen I; 2) validate the gene array data for transgelin, the most highly dysregulated gene in PSCs grown on activating vs. nonactivating matrices, at mRNA and protein levels; 3) examine the role of transgelin in PSC function; and 4) assess transgelin expression in human chronic pancreatitis sections. Culture of PSCs on different matrices significantly affected their gene expression pattern. 146, 619, and 432 genes, respectively, were differentially expressed ( P < 0.001) in PSCs cultured on collagen I vs. Matrigel, Matrigel vs. plastic, and collagen I vs. plastic. The highest fold change (12.5-fold upregulation) in gene expression in cells on collagen I vs. Matrigel was observed for transgelin (an actin stress fiber-associated protein). Transgelin was significantly increased in activated PSCs vs. quiescent PSCs. Silencing transgelin expression decreased PSC proliferation and also reduced platelet-derived growth factor-induced PSC migration. Notably, transgelin was highly expressed in chronic pancreatitis in stromal areas and periacinar spaces but was absent in acinar cells. These findings suggest that transgelin is a potentially useful target protein to modulate PSC function so as to ameliorate pancreatic fibrosis.

Interactions between cadmium and zinc on gene expression pattern of differentiation markers in MC3T3-E1 cell line

Xenobiotica ◽  
2021 ◽  
pp. 1-28
Author(s):  
Sana Boughammoura ◽  
Mylène Zarka ◽  
Imed Messaoudi ◽  
Martine Cohen Solal
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Differentiation Markers
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