scholarly journals Microarray expression profiling in the denervated hippocampus identifies long noncoding RNAs functionally involved in neurogenesis

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Bingying Deng ◽  
Xiang Cheng ◽  
Haoming Li ◽  
Jianbing Qin ◽  
Meiling Tian ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Liang Tang ◽  
Lan Liu ◽  
Guangyi Li ◽  
Pengcheng Jiang ◽  
Yan Wang ◽  
...  

Alzheimer’s disease (AD), characterized by memory loss, cognitive decline, and dementia, is a progressive neurodegenerative disease. Although the long noncoding RNAs (lncRNAs) have recently been identified to play a role in the pathogenesis of AD, the specific effects of lncRNAs in AD remain unclear. In present study, we have investigated the expression profiles of lncRNAs in hippocampal of intranasal LPS-mediated Alzheimer’s disease models in mice by microarray method. A total of 395 lncRNAs and 123 mRNAs was detected to express differently in AD models and controls (>2.0 folds,p<0.05). The microarray expression was validated by Quantitative Real-Time-PCR (qRT-PCR). The pathway analysis showed the mRNAs that correlated with lncRNAs were involved in inflammation, apoptosis, and nervous system related pathways. The lncRNA-TFs network analysis suggested the lncRNAs were mostly regulated by HMGA2, ONECUT2, FOXO1, and CDC5L. Additionally, lncRNA-target-TFs network analysis indicated the FOXL1, CDC5L, ONECUT2, and CDX1 to be the TFs most likely to regulate the production of these lncRNAs. This is the first study to investigate lncRNAs expression pattern in intranasal LPS-mediated Alzheimer’s disease model in mice. And these results may facilitate the understanding of the pathogenesis of AD targeting lncRNAs.


2001 ◽  
Vol 12 (10) ◽  
pp. 758-764 ◽  
Author(s):  
Jonathan D. Choi ◽  
Lara A. Underkoffler ◽  
Joelle N. Collins ◽  
Shannon M. Marchegiani ◽  
Natalie A. Terry ◽  
...  

2004 ◽  
Vol 19 (3) ◽  
pp. 319-330 ◽  
Author(s):  
Harry Björkbacka ◽  
Katherine A. Fitzgerald ◽  
François Huet ◽  
Xiaoman Li ◽  
James A. Gregory ◽  
...  

Myeloid differentiation protein-88 (MyD88) is a signal adaptor protein required for cytokine production following engagement of Toll-like receptors (TLRs) by their cognate ligands. Activation of both TLR-3 and TLR-4, however, can engage signaling events independent of MyD88 expression. The relative importance of these MyD88-dependent and -independent signaling pathways in the macrophage response to lipopolysaccharide (LPS) is unknown. Here we define these events using microarray expression profiling of LPS-stimulated macrophages taken from MyD88-null and wild-type mice. Of the 1,055 genes found to be LPS responsive, only 21.5% were dependent on MyD88 expression, with MyD88-independent genes constituting 74.7% of the genetic response. This MyD88-independent gene expression was predominantly transcriptionally regulated, as it was unaffected by cycloheximide blockade of new protein synthesis. A previously undescribed group of LPS-regulated genes (3.8%), whose induction or repression was significantly greater in the absence of MyD88, was also identified by these studies. The regulation of these genes suggested that MyD88 could serve as a molecular brake, constraining gene activity in a subset of LPS-responsive genes. The findings generated with LPS stimulation were recapitulated by exposure of macrophages to live Escherichia coli. These expression-profiling studies redefine the current dogma of TLR-4 signaling and establish that MyD88, although essential for some of the best-characterized macrophage responses to LPS, is not required for the regulation of the majority of genes engaged by macrophage exposure to endotoxin or live bacteria.


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