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Ependymoma in Childhood and Adolescence
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Gain of 9qter has been associated with recurrent tumor and candidate gene expression analysis in these loci revealed upregulation of two oncogenes of significance, Notch1 and TNC.72 Members of the notch signaling pathway were upregulated, including overexpression of its receptors (Notch1, Notch2), ligands (DLL1, DLL3, JAG1, JAG2), downstream mediators (HES1, HEY2, c-Myc), and suppression of ubiquitin-dependent, proteolytic mediator of Notch1 (FBXW7). Notch signaling regulates cell fate during development, proliferation, differentiation, and apoptosis, and has been implicated in tumorigenesis of other brain tumors, including embryonal tumors.73 The importance of Notch signaling in pediatric as opposed to adult ependymoma is uncertain.74
Nidus or no nidus: Is it a crucial issue for diagnostic assessment of arteriovenous malformations?
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
Expression of specific markers in endothelial cells determines their differentiation, either into an artery or into a vein in the early stage of vascular development.4, 5 The Dll4-Hey2-EphrinB2 pathway determines endothelial fate as an artery, and the COUP-TFII pathway signals endothelial cells to become veins.6, 7
Notch promotes DNMT-mediated hypermethylation of Klotho leads to COPD-related inflammation
Published in Experimental Lung Research, 2018
Jie Qiu, Ya-Nan Zhang, Xiwei Zheng, Peng Zhang, Gang Ma, Hai Tan
Notch signaling pathway is the most fundamental system in mammalian, related with a variety of basic biological functions and tumorigenesis. Previous study reported the active Notch1 and Hey2 expression increased in COPD patients, especially in the position of goblet-cell metaplasia and in submucosal glands,41 indicating that the Notch signaling pathway might be involved in the process of COPD development. In our research, we found that CSE induced Notch signaling activation (Figure 2C), which was consistent with the mentioned study. Furthermore, we also found that DNMTs-mediated CpG methylation depended on Notch signaling activation (Figure 2C, right panel). These results first combined Notch signaling with CpG methylation. As the regulation of gene expression by DNA methylation comprises quite complex mechanisms, Notch activation may affect CpG methylation through affecting unknown factors or directly affect DNMTs activity. Few researches focused on the interaction between Notch signal factors and DNMTs, and more evidences are required to investigate the mechanism of Notch participating in CpG methylation. Cell apoptosis and sustain inflammatory responses may be responsible for the development of emphysema.42 In Figures 3 and 4, we showed that both Notch signaling and DNMTs-mediated methylation were necessary in the process of COPD deterioration. Besides the well-known effect of Notch on inflammation, these findings provided a new insight into the role of the Notch pathway in COPD.
Diverse endometrial mRNA signatures during the window of implantation in patients with repeated implantation failure
Published in Human Fertility, 2018
Cheng Shi, Hong Jing Han, Li Juan Fan, Jing Guan, Xing Bang Zheng, Xi Chen, Rong Liang, Xiao Wei Zhang, Kun Kun Sun, Qing Hua Cui, Huan Shen
In the first category, studies on fertile women’s natural cycles, the ERA developed by Diaz-Gimeno et al. (2011) and the receptivity associated genes (RAGs) reported by Bhagwat et al. (2013) provided two lists of well-established genes which were differentially expressed in the transition from non-WOI to WOI endometrium. Comparing the 357 differentially expressed genes with the 238 genes listed in ERA, 35 identical genes were located. Furthermore, among these 35 genes, 19 genes up-regulated during the WOI in the ERA were down-regulated in the RIF group (AQP3, ASS1, CLU, DHRS3, DPP4, GAS1, GAST, GPX3, HABP2, IGFBP1, IMPA2, LEPREL1, NNMT, PROM1, RARRES1, SERPING1, SYNE2, THBS2, TIMP3); while the other 16 genes that were down-regulated during the WOI were up-regulated in the RIF group (TTC21B, ANK3, ADAMTS8, CAPN6, CTNNA2, EDN3, HEY2, HLADOB, IDH1, KCNG1, LRRC1, LRRC17, NDRG2, SFRP4, SOX17, STEAP4). Twenty-three of the differentially expressed genes were also found in the RAGs list, while 21 of them gave the same trend as mentioned above (GPX3, DPP4, CXCR4, DHRS3, TGM2, RARRES1, C9orf71, TIMP3, CLU, AQP3, THBS2, TNFAIP2, GPR110, CATSPERB, HABP2, PROM1, IMPA2, GAST, IGFBP1, ABP1 and KCNG1) (Table 5). Such consistency indicated that these genes were not only correlated to endometrial receptivity but could result in implantation failure if they were not expressed appropriately.
The Notch pathway: a novel therapeutic target for cardiovascular diseases?
Published in Expert Opinion on Therapeutic Targets, 2019
Giorgio Aquila, Aleksandra Kostina, Francesco Vieceli Dalla Sega, Eugeniy Shlyakhto, Anna Kostareva, Luisa Marracino, Roberto Ferrari, Paola Rizzo, Anna Malaschicheva
The sequential expression of components of the Notch pathways and related genes is indispensable during the development of heart and vessels. The role of Notch in the cardiovascular development has been deeply investigated and its discussion is beyond the scope of this review: we give here a brief overview of the field, to set the stage for our discussion of the role of Notch in cardiovascular disease, and refer the reader to several excellent reviews for details [25–27]. Notch ligands and receptors are sequentially expressed in the developing heart, thus ensuring proper heart development. Notch ligand Jagged1 is expressed very early during heart development, labeling the presumptive valve area of the atrioventricular channel (AVC) and the trabecular myocardium, while ligand Dll4 and receptors Notch2 and Notch4 are expressed in the endocardium. Then, Dll4 expression decreases whereas Jagged1 expression is maintained in the endocardium and is activated in the compacted myocardium [25,28]. This sequential expression of Notch genes Jagged1, Dll4, Notch2 and Notch4 supports myocardial patterning, maturation and compaction and cardiac trabeculae formation [25,28]. The Notch pathway plays an important role in the development of outflow tract (OFT) of the heart which starts with endothelial-to-mesenchymal transition (EMT) in the endocardial cells leading to the formation of cardiac valves. The involvement of Notch1 in this context is indicated by the expression of this receptor in prospective valve endocardium at the beginning of EMT [29]. Consistently with the importance of Notch in the developing heart, mice lacking Notch target genes Hey1 and Hey2 die during embryogenesis due to severe cardiovascular malformations, including impaired development of EMT [30].