Analysis of genes involved in cell proliferation, adhesion, and control of apoptosis during embryonic neurogenesis in Induced Pluripotent Stem Cells (iPSCs) from patients with Focal Cortical Dysplasia

2020 ◽  
Vol 155 ◽  
pp. 112-118 ◽  
Author(s):  
Daniel Rodrigo Marinowic ◽  
Fernanda Majolo ◽  
Gabriele Goulart Zanirati ◽  
Ismael Plentz ◽  
Eliseu Paglioli Neto ◽  
...  
Neuroscience ◽  
2019 ◽  
Vol 408 ◽  
pp. 81-90 ◽  
Author(s):  
Fernanda Majolo ◽  
Daniel Rodrigo Marinowic ◽  
André Luis Fernandes Palmini ◽  
Jaderson Costa DaCosta ◽  
Denise Cantarelli Machado

2017 ◽  
Vol 15 (4) ◽  
pp. 2049-2056 ◽  
Author(s):  
Daniel Rodrigo Marinowic ◽  
Fernanda Majolo ◽  
Alessandra Deise Sebben ◽  
Vinicius Duval Da Silva ◽  
Tiago Giuliani Lopes ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Yanan Zhang ◽  
Huan Liu ◽  
Xialu Lin ◽  
Feng’e Zhang ◽  
Peilin Meng ◽  
...  

Kashin–Beck disease (KBD) mainly damages growth plate of adolescents and is susceptible to both gene and gene–environmental risk factors. HT-2 toxin, which is a primary metabolite of T-2 toxin, was regarded as one of the environmental risk factors of KBD. We used successfully generated KBD human induced pluripotent stem cells (hiPSCs) and control hiPSCs, which carry different genetic information. They have potential significance in exploring the effects of HT-2 toxin on hiPSC chondrocytes and interactive genes with HT-2 toxin for the purpose of providing a cellular disease model for KBD. In this study, we gave HT-2 toxin treatment to differentiating hiPSC chondrocytes in order to investigate the different responses of KBD hiPSC chondrocytes and control hiPSC chondrocytes to HT-2 toxin. The morphology of HT-2 toxin-treated hiPSC chondrocytes investigated by transmission electron microscope clearly showed that the ultrastructure of organelles was damaged and type II collagen expression in hiPSC chondrocytes was downregulated by HT-2 treatment. Moreover, dysregulation of cell cycle was observed; and p53, p21, and CKD6 gene expressions were dysregulated in hiPSC chondrocytes after T-2 toxin treatment. Flow cytometry also demonstrated that there were significantly increased amounts of late apoptotic cells in KBD hiPSC chondrocytes and that the mRNA expression level of Fas was upregulated. In addition, KBD hiPSC chondrocytes presented stronger responses to HT-2 toxin than control hiPSC chondrocytes. These findings confirmed that HT-2 is an environmental risk factor of KBD and that p53 pathway interacted with HT-2 toxin, causing damaged ultrastructure of organelles, accelerating cell cycle in G1 phase, and increasing late apoptosis in KBD hiPSC chondrocytes.


PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11388
Author(s):  
Panetha Pansri ◽  
Phetcharat Phanthong ◽  
Nopparat Suthprasertporn ◽  
Yindee Kitiyanant ◽  
Alisa Tubsuwan ◽  
...  

Background Several pieces of evidence from in vitro studies showed that brain-derived neurotrophic factor (BDNF) promotes proliferation and differentiation of neural stem/progenitor cells (NSCs) into neurons. Moreover, the JAK2 pathway was proposed to be associated with mouse NSC proliferation. BDNF could activate the STAT-3 pathway and induce proliferation in mouse NSCs. However, its effects on proliferation are not fully understood and JAK/STAT pathway was proposed to play a role in this activity. Methods In the present study, the effects of BDNF on cell proliferation and neurite outgrowth of Alzheimer’s disease (AD) induced pluripotent stem cells (iPSCs)-derived human neural progenitor cells (hNPCs) were examined. Moreover, a specific signal transduction pathway important in cell proliferation was investigated using a JAK2 inhibitor (AG490) to clarify the role of that pathway. Results The proliferative effect of BDNF was remarkably observed as an increase in Ki-67 positive cells. The cell number of hNPCs was significantly increased after BDNF treatment represented by cellular metabolic activity of the cells measured by MTT assay. This noticeable effect was statistically shown at 20 ng/ml of BDNF treatment. BDNF, however, did not promote neurite outgrowth but increased neuronal cell number. It was found that AG490 suppressed hNPCs proliferation. However, this inhibitor partially decreased BDNF-induced hNPCs proliferation. These results demonstrated the potential role of BDNF for the amelioration of AD through the increase of AD-derived hNPCs number.


2010 ◽  
Vol 34 (8) ◽  
pp. S36-S36
Author(s):  
Ping Duan ◽  
Xuelin Ren ◽  
Wenhai Yan ◽  
Xuefei Han ◽  
Xu Yan ◽  
...  

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