scholarly journals ProNGF Is a Cell-Type-Specific Mitogen for Adult Hippocampal and for Induced Neural Stem Cells

Stem Cells ◽  
2019 ◽  
Vol 37 (9) ◽  
pp. 1223-1237 ◽  
Author(s):  
Valerio Corvaglia ◽  
Domenica Cilli ◽  
Chiara Scopa ◽  
Rossella Brandi ◽  
Ivan Arisi ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3365
Author(s):  
Gabriela Maria Guerra ◽  
Doreen May ◽  
Torsten Kroll ◽  
Philipp Koch ◽  
Marco Groth ◽  
...  

SMG6 is an endonuclease, which cleaves mRNAs during nonsense-mediated mRNA decay (NMD), thereby regulating gene expression and controling mRNA quality. SMG6 has been shown as a differentiation license factor of totipotent embryonic stem cells. To investigate whether it controls the differentiation of lineage-specific pluripotent progenitor cells, we inactivated Smg6 in murine embryonic neural stem cells. Nestin-Cre-mediated deletion of Smg6 in mouse neuroprogenitor cells (NPCs) caused perinatal lethality. Mutant mice brains showed normal structure at E14.5 but great reduction of the cortical NPCs and late-born cortical neurons during later stages of neurogenesis (i.e., E18.5). Smg6 inactivation led to dramatic cell death in ganglionic eminence (GE) and a reduction of interneurons at E14.5. Interestingly, neurosphere assays showed self-renewal defects specifically in interneuron progenitors but not in cortical NPCs. RT-qPCR analysis revealed that the interneuron differentiation regulators Dlx1 and Dlx2 were reduced after Smg6 deletion. Intriguingly, when Smg6 was deleted specifically in cortical and hippocampal progenitors, the mutant mice were viable and showed normal size and architecture of the cortex at E18.5. Thus, SMG6 regulates cell fate in a cell type-specific manner and is more important for neuroprogenitors originating from the GE than for progenitors from the cortex.



2018 ◽  
Vol 14 (2) ◽  
pp. 95-102 ◽  
Author(s):  
Yunzhao Gu ◽  
Jun Wu ◽  
Wenxiao Yang ◽  
Chao Xia ◽  
Xinglong Shi ◽  
...  

LIF-mediated STAT3 signaling contributes to proliferation and exhibits a cell-specific binding pattern in mouse female germline stem cells.



2013 ◽  
Vol 26 (1) ◽  
pp. 101-112 ◽  
Author(s):  
Tony D. Southall ◽  
Katrina S. Gold ◽  
Boris Egger ◽  
Catherine M. Davidson ◽  
Elizabeth E. Caygill ◽  
...  


2021 ◽  
Author(s):  
yuanyuan wang ◽  
mingyan lin

The pathology underlying schizophrenia (SCZ) involves cell type-specific and developmental stage-specific dysregulation of multiple gene regulatory networks dominated by some key transcription factors, such as SCZ risk gene transcription factor 4 (TCF4). Previous studies on the regulatory mechanism of TCF4 use SY5Y as the cellular model, which could not reflect its cell type-specific role in the real world. Using the transcriptional profile of whole brain during development stages and single-cell transcriptome data in the developing human prefrontal cortex, we found that TCF4 was preferentially expressed in the interneuron. Chromatin immunoprecipitation combined with sequencing (ChIP-Seq) in human embryonic stem cells (hESC)-derived interneurons revealed that TCF4 primarily activate transcription of genes associated with cortex development and telencephalon regionalization in a long-range manner. As expected, the downstream targets of TCF4 were distinct in inhibitory neurons and neural stem cells during early neurodevelopment, justifying the importance of our study. Deeper investigation further revealed that TCF4 regulate genes related to neurotransmission distally in interneuron in a c-FOS dependent manner, while TCF4 and TCF3 synergistically regulate genes associated with cell proliferation associated proximally in neural stem cells. Our findings suggested that defects in development of interneuron, for instance as a result of TCF4 abnormality, may break excitation and inhibition balance and contribute significantly to the risk of SCZ.



2014 ◽  
Vol 45 ◽  
pp. 192-200 ◽  
Author(s):  
Nasir Malik ◽  
Anastasia G. Efthymiou ◽  
Karly Mather ◽  
Nathaniel Chester ◽  
Xiantao Wang ◽  
...  


2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg


2020 ◽  
Vol 528 (13) ◽  
pp. 2218-2238 ◽  
Author(s):  
Attilio Iemolo ◽  
Patricia Montilla‐Perez ◽  
I‐Chi Lai ◽  
Yinuo Meng ◽  
Syreeta Nolan ◽  
...  


2013 ◽  
Vol 28 (3) ◽  
pp. 267-273 ◽  
Author(s):  
Marica Gemei ◽  
Rosa Di Noto ◽  
Peppino Mirabelli ◽  
Luigi Del Vecchio

In colorectal cancer, CD133+ cells from fresh biopsies proved to be more tumorigenic than their CD133– counterparts. Nevertheless, the function of CD133 protein in tumorigenic cells seems only marginal. Moreover, CD133 expression alone is insufficient to isolate true cancer stem cells, since only 1 out of 262 CD133+ cells actually displays stem-cell capacity. Thus, new markers for colorectal cancer stem cells are needed. Here, we show the extensive characterization of CD133+ cells in 5 different colon carcinoma continuous cell lines (HT29, HCT116, Caco2, GEO and LS174T), each representing a different maturation level of colorectal cancer cells. Markers associated with stemness, tumorigenesis and metastatic potential were selected. We identified 6 molecules consistently present on CD133+ cells: CD9, CD29, CD49b, CD59, CD151, and CD326. By contrast, CD24, CD26, CD54, CD66c, CD81, CD90, CD99, CD112, CD164, CD166, and CD200 showed a discontinuous behavior, which led us to identify cell type-specific surface antigen mosaics. Finally, some antigens, e.g. CD227, indicated the possibility of classifying the CD133+ cells into 2 subsets likely exhibiting specific features. This study reports, for the first time, an extended characterization of the CD133+ cells in colon carcinoma cell lines and provides a “dictionary” of antigens to be used in colorectal cancer research.



2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii88-ii88
Author(s):  
Alison Mercer-Smith ◽  
Wulin Jiang ◽  
Alain Valdivia ◽  
Juli Bago ◽  
Scott Floyd ◽  
...  

Abstract INTRODUCTION Non-small cell lung cancer (NSCLC) is the most common cancer to form brain metastases. Radiation treatment is standard-of-care, but recurrence is still observed in 40% of patients. An adjuvant treatment is desperately needed to track down and kill tumor remnants after radiation. Tumoritropic neural stem cells (NSCs) that can home to and deliver a cytotoxic payload offer potential as such an adjuvant treatment. Here we show the transdifferentiation of human fibroblasts into tumor-homing induced neural stem cells (hiNSCs) that secrete the cytotoxic protein TRAIL (hiNSC-TRAIL) and explore the use of hiNSC-TRAIL to treat NSCLC brain metastases. METHODS To determine the migratory capacity of hiNSCs, hiNSCs were infused intracerebroventricularly (ICV) into mice bearing established bilateral NSCLC H460 brain tumors. hiNSC accumulation at tumor foci was monitored using bioluminescent imaging and post-mortem fluorescent analysis. To determine synergistic effects of radiation with TRAIL on NSCLC, we performed in vitro co-culture assays and isobologram analysis. In vivo, efficacy was determined by tracking the progression and survival of mice bearing intracranial H460 treated with hiNSC-TRAIL alone or in combination with 2 Gy radiation. RESULTS/CONCLUSION Following ICV infusion, hiNSCs persisted in the brain for > 1 week and migrated from the ventricles to colocalize with bilateral tumor foci. In vitro, viability assays and isobologram analysis revealed the combination treatment of hiNSC-TRAIL and 2 Gy radiation induced synergistic killing (combination index=0.64). In vivo, hiNSC-TRAIL/radiation combination therapy reduced tumor volumes > 90% compared to control-treated animals while radiation-only and hiNSC-TRAIL-only treated mice showed 21% and 52% reduced volumes, respectively. Dual-treatment extended survival 40%, increasing survival from a median of 20 days in controls to 28 days in the treatment group. These results suggest hiNSC-TRAIL can improve radiation therapy for NSCLC brain metastases and could potentially improve outcomes for patients suffering from this aggressive form of cancer.



2017 ◽  
Vol 381 ◽  
pp. 286
Author(s):  
G. Davaa ◽  
J.Y. Hong ◽  
J. Olmos Buitrago ◽  
H.W. Kim ◽  
J.K. Hyun


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