Corrigendum to “Neuropeptide Y is important for basal and seizure-induced precursor cell proliferation in the hippocampus” [Neurobiol. Dis. 26/1 (2007) 174–188]

2013 ◽  
Vol 49 ◽  
pp. 199
Author(s):  
Owain W. Howell ◽  
Sharmalene Silva ◽  
Helen E. Scharfman ◽  
Alexander A. Sosunov ◽  
Malik Zaben ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuropeptide Y ◽  
Precursor Cell

Neuropeptide Y is important for basal and seizure-induced precursor cell proliferation in the hippocampus

2007 ◽  
Vol 26 (1) ◽  
pp. 174-188 ◽  
Author(s):  
Owain W. Howell ◽  
Sharmalene Silva ◽  
Helen E. Scharfman ◽  
Alexander A. Sosunov ◽  
Malik Zaben ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuropeptide Y ◽  
Precursor Cell

scholarly journals Neuropeptide Y (NPY) promotes inflammation-induced tumorigenesis by enhancing epithelial cell proliferation

2017 ◽  
Vol 312 (2) ◽  
pp. G103-G111 ◽  
Author(s):  
Sabrina Jeppsson ◽  
Shanthi Srinivasan ◽  
Bindu Chandrasekharan
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Neuropeptide Y ◽  
Intestinal Inflammation ◽  
Enteric Neurons ◽  
Intestinal Epithelial ◽  
Epithelial Proliferation ◽  
Proliferation And Apoptosis

We have demonstrated that neuropeptide Y (NPY), abundantly produced by enteric neurons, is an important regulator of intestinal inflammation. However, the role of NPY in the progression of chronic inflammation to tumorigenesis is unknown. We investigated whether NPY could modulate epithelial cell proliferation and apoptosis, and thus regulate tumorigenesis. Repeated cycles of dextran sodium sulfate (DSS) were used to model inflammation-induced tumorigenesis in wild-type (WT) and NPY knockout ( NPY−/−) mice. Intestinal epithelial cell lines (T84) were used to assess the effects of NPY (0.1 µM) on epithelial proliferation and apoptosis in vitro. DSS-WT mice exhibited enhanced intestinal inflammation, polyp size, and polyp number (7.5 ± 0.8) compared with DSS- NPY−/− mice (4 ± 0.5, P < 0.01). Accordingly, DSS-WT mice also showed increased colonic epithelial proliferation (PCNA, Ki67) and reduced apoptosis (TUNEL) compared with DSS- NPY−/− mice. The apoptosis regulating microRNA, miR-375, was significantly downregulated in the colon of DSS-WT (2-fold, P < 0.01) compared with DSS- NPY−/−-mice. In vitro studies indicated that NPY promotes cell proliferation (increase in PCNA and β-catenin, P < 0.05) via phosphatidyl-inositol-3-kinase (PI3-K)-β-catenin signaling, suppressed miR-375 expression, and reduced apoptosis (increase in phospho-Bad). NPY-treated cells also displayed increased c-Myc and cyclin D1, and reduction in p21 ( P < 0.05). Addition of miR-375 inhibitor to cells already treated with NPY did not further enhance the effects induced by NPY alone. Our findings demonstrate a novel regulation of inflammation-induced tumorigenesis by NPY-epithelial cross talk as mediated by activation of PI3-K signaling and downregulation of miR-375. NEW & NOTEWORTHY Our work exemplifies a novel role of neuropeptide Y (NPY) in regulating inflammation-induced tumorigenesis via two modalities: first by enhanced proliferation (PI3-K/pAkt), and second by downregulation of microRNA-375 (miR-375)-dependent apoptosis in intestinal epithelial cells. Our data establish the existence of a microRNA-mediated cross talk between enteric neurons producing NPY and intestinal epithelial cells, and the potential of neuropeptide-regulated miRNAs as potential therapeutic molecules for the management of inflammation-associated tumors in the gut.

scholarly journals Oncogenes - the basics

2018 ◽  
Vol 3 (4) ◽  
pp. 35-37
Author(s):  
Arnab Ghosh ◽  
Diasma Ghartimagar ◽  
Sushma Thapa
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Normal Cell ◽  
Tumor Formation ◽  
Precursor Cell ◽  
Single Precursor ◽  
Normal Cell Cycle

Normal cell cycle and cell proliferation are regulated by several genes which can be broadly classified into 4 groups viz, proto-oncogenes, tumor suppressor genes, genes regulating apoptosis and genes involved in DNA repair. These genes may be defective due to different factors. The defective genes may lead to production of abnormal proteins which may lead to disruption of the normal cell cycle and proliferation. A single precursor cell with defective gene proliferates surpassing the normal physiologic regulatory process and leads to tumor formation, so, traditionally,it is said that “tumors are clonal”.

scholarly journals Nox4 Promotes Neural Stem/Precursor Cell Proliferation and Neurogenesis in the Hippocampus and Restores Memory Function Following Trimethyltin-Induced Injury

Neuroscience ◽  
2019 ◽  
Vol 398 ◽  
pp. 193-205 ◽  
Author(s):  
Yoji Yoshikawa ◽  
Tetsuro Ago ◽  
Junya Kuroda ◽  
Yoshinobu Wakisaka ◽  
Masaki Tachibana ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Memory Function ◽  
Precursor Cell

scholarly journals Stabilized β-Catenin Functions through TCF/LEF Proteins and the Notch/RBP-Jκ Complex To Promote Proliferation and Suppress Differentiation of Neural Precursor Cells

2008 ◽  
Vol 28 (24) ◽  
pp. 7427-7441 ◽  
Author(s):  
Takeshi Shimizu ◽  
Tetsushi Kagawa ◽  
Toshihiro Inoue ◽  
Aya Nonaka ◽  
Shinji Takada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuronal Differentiation ◽  
Glycogen Synthase ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Self Renewal ◽  
Fgf Receptor ◽  
Proliferation And Differentiation

ABSTRACT The proliferation and differentiation of neural precursor cells are mutually exclusive during brain development. Despite its importance for precursor cell self renewal, the molecular linkage between these two events has remained unclear. Fibroblast growth factor 2 (FGF2) promotes neural precursor cell proliferation and concurrently inhibits their differentiation, suggesting a cross talk between proliferation and differentiation signaling pathways downstream of the FGF receptor. We demonstrate that FGF2 signaling through phosphatidylinositol 3 kinase activation inactivates glycogen synthase kinase 3β (GSK3β) and leads to the accumulation of β-catenin in a manner different from that in the Wnt canonical pathway. The nuclear accumulated β-catenin leads to cell proliferation by activating LEF/TCF transcription factors and concurrently inhibits neuronal differentiation by potentiating the Notch1-RBP-Jκ signaling pathway. β-Catenin and the Notch1 intracellular domain form a molecular complex with the promoter region of the antineurogenic hes1 gene, allowing its expression. This signaling interplay is especially essential for neural stem cell maintenance, since the misexpression of dominant-active GSK3β completely inhibits the self renewal of neurosphere-forming stem cells and prompts their neuronal differentiation. Thus, the GSK3β/β-catenin signaling axis regulated by FGF and Wnt signals plays a pivotal role in the maintenance of neural stem/precursor cells by linking the cell proliferation to the inhibition of differentiation.

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