scholarly journals Loss of ARNT/HIF1β Mediates Altered Gene Expression and Pancreatic-Islet Dysfunction in Human Type 2 Diabetes

Cell ◽  
2005 ◽  
Vol 122 (3) ◽  
pp. 337-349 ◽  
Author(s):  
Jenny E. Gunton ◽  
Rohit N. Kulkarni ◽  
SunHee Yim ◽  
Terumasa Okada ◽  
Wayne J. Hawthorne ◽  
...  
Author(s):  
Nawal Helmi ◽  
Dalia Alammari ◽  
Mohammad Mobashir

Background: Coronavirus is an enveloped positive-sense RNA virus and is characterized by club-like spikes projecting from its surface which is commonly associated with acute respiratory infections in humans but its ability to infect multiple host species and multiple diseases brings it to a complex pathogen group. The frequent interactions of wild animals with humans it is more prevalent a common source of such infections and SARS—CoV and MERS—CoV are the zoonotic pathogens among the leading cause of severe respiratory diseases in humans. Aim: The major purpose of this study was to study the gene expression profiling for those human samples which are infected with coronavirus or uninfected and compare the differential expression patterns and its functional impact. Methods: For this purpose, the previously studied samples have been collected from public database and the study had been performed and it includes gene expression analysis, pathway analysis, and the network-level understanding. The analysis presents the data for the differentially expressed genes, enriched pathways and the networks for the potential genes and gene sets. In terms of gene expression and the linkage of COVID-19 with type-2 diabetes. Results: We observe that there are a large number of genes which show altered gene expression pattern than the normal for coronavirus infection while in terms of pathways it appears that there are few sets of functions which are affected due to altered gene expression and they infer to infection, inflammation, and the immune system. Conclusions: Based on our study, we conclude that the potential genes which are affected due to infection are NFKBIA, MYC, FOXO3, BIRC3, ICAM1, IL8, CXCL1/2/5, GADD45A, RELB, SGK1, AREG, BBC3, DDIT3/4, EGR1, MTHFD2, and SESN2 and the functional changes are mainly associated with these pathways TNF, cytokine, NF—kB, TLR, TCR, BCR, Foxo, and TGF signaling pathways are among them and there are additional pathways such as hippo signaling, apoptosis, estrogen signaling, regulating pluropotency of stem cells, ErbB, Wnt, p53, cAMP, MAPK, PI3K—AKT, oxidative phosphorylation, protein processing in endoplasmic reticulum, prolactin signaling, adipocytokine, neurotrophine signaling, and longevity regulating pathways. SMARCD3, PARL, GLIPR1, STAT2, PMAIP1, GP1BA, and TOX genes and PI3K-Akt, focal adhesion, Foxo, phagosome, adrenergic, osteoclast differentiation, platelet activation, insulin, cytokine-cytokine interaction, apoptosis, ECM, JAK-STAT, and oxytocine signaling appear as the linkage between COVID-19 and Type-2 diabetes.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Andreas Buch Møller ◽  
Ulla Kampmann ◽  
Jakob Hedegaard ◽  
Kasper Thorsen ◽  
Iver Nordentoft ◽  
...  

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Shunsuke Omodaka ◽  
Atsushi Kanoke ◽  
Suwei Wong ◽  
Dvir Aran ◽  
Jialing Liu

Introduction: Type 2 diabetes mellitus (T2DM) is associated with poor outcome after stroke. Brain myeloid cells are considered to play a pivotal role in modulating brain damage and recovery after stroke, but how myeloid response to stroke under diabetic condition is largely unclear. We used single-cell RNA sequencing (scRNA seq) to determine the transcriptome profiles of brain myeloid cells under diabetic and ischemic conditions using T2DM mouse model. Hypothesis: The altered gene expression in the brain myeloid cells under diabetic condition leads to the aggravation of ischemic brain injury. Methods: We performed scRNA seq in Percoll gradient-isolated brain mononuclear cells from middle-aged db/db and db/+ mice three days after direct middle cerebral artery occlusion (MCAO) or sham-operation. Clusters of brain myeloid cells were predominantly annotated as macrophages (mp) or microglia (mg) according to the expression of marker genes in each cell type. We identified DM-unique differentially expressed genes (DEGs) and stroke-unique DEGs, and assessed the biological role of these DEGs by enrichment analysis. Results: Myeloid cell population was increased in DM ( db/db without MCAO; mp 37.3% mg 10.6%) and stroke ( db/+ with MCAO; mp 26.2% mg 33.2%) group compared to control ( db/+ without MCAO; mp 3.4% mg 0.8%) group. In macrophages, 91 DM-unique (64 up- and 27 down-regulated) and 464 stroke-unique (458 up- and 6 down-regulated) DEGs were identified, whereas 258 stroke-unique (254 up- and 4 down-regulated) DEGs were identified in microglia. Enrichment analysis revealed that DM-unique down-regulated DEGs in macrophages were related to MHC class II antigen processing involved in Staphylococcus aureus infection pathway, indicating a possible relationship between immunosuppression and stroke aggravation in diabetes. DM-unique and stroke-unique up-regulated DEGs were related to oxidative phosphorylation, phagocytosis, and protein metabolism. Conclusions: The present study demonstrated altered gene expression profile and molecular network of brain myeloid cells in response to diabetic and ischemic conditions by scRNA seq, providing a clue to the underlying mechanism of the adverse effect of T2DM on stroke.


BMC Genomics ◽  
2012 ◽  
Vol 13 (1) ◽  
pp. 81 ◽  
Author(s):  
Omar Abdul-Rahman ◽  
Maria Sasvari-Szekely ◽  
Agota Ver ◽  
Klara Rosta ◽  
Bernadett K Szasz ◽  
...  

Author(s):  
W. K. Jones ◽  
J. Robbins

Two myosin heavy chains (MyHC) are expressed in the mammalian heart and are differentially regulated during development. In the mouse, the α-MyHC is expressed constitutively in the atrium. At birth, the β-MyHC is downregulated and replaced by the α-MyHC, which is the sole cardiac MyHC isoform in the adult heart. We have employed transgenic and gene-targeting methodologies to study the regulation of cardiac MyHC gene expression and the functional and developmental consequences of altered α-MyHC expression in the mouse.We previously characterized an α-MyHC promoter capable of driving tissue-specific and developmentally correct expression of a CAT (chloramphenicol acetyltransferase) marker in the mouse. Tissue surveys detected a small amount of CAT activity in the lung (Fig. 1a). The results of in situ hybridization analyses indicated that the pattern of CAT transcript in the adult heart (Fig. 1b, top panel) is the same as that of α-MyHC (Fig. 1b, lower panel). The α-MyHC gene is expressed in a layer of cardiac muscle (pulmonary myocardium) associated with the pulmonary veins (Fig. 1c). These studies extend our understanding of α-MyHC expression and delimit a third cardiac compartment.


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