Neuronal Precursor Cell Proliferation on Elastic Substrates

Author(s):  
Michelle L. Previtera ◽  
Mason Hui ◽  
Malav Desai ◽  
Devendra Verma ◽  
Rene Schloss ◽  
...  

Numerous stem cells therapies have been studied for the replacement of damaged neurons due to spinal cord injury. Our laboratory’s goal is to design an implantable platform for spinal cord neuron (SCN) proliferation and differentiation in order to replace damaged neurons in the injured spinal cord. Based on previous literature, we suspect we can promote neuronal precursor cell (NPC) proliferation and differentiation utilizing elastic matrices.

Author(s):  
Mohamed Ismail ◽  
Sara Ibrahim ◽  
Azza Elamir ◽  
Amira M. Elrafei ◽  
Nageh Allam ◽  
...  

Implantable drug-delivery systems provide new means for achieving therapeutic drug concentration over a prolonged time to achieve better tissue protection and enhanced recovery. The hypothesis of the current study was to test the antioxidant and anti-inflammatory effects of genistein and nanofibers on the spinal cord tissue following experimental spinal cord injury (SCI). Rats were treated post SCI with genistein loaded on chitosan/polyvinyl alcohol (CS/PVA) nanofibers as an implantable drug-delivery system. SCI caused marked oxidative damage and inflammation as evident by the reduction in the super oxide dismutase (SOD) activity and the level of interleukin-10 (IL-10) in injured spinal cord tissue, as well as, the significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF-α). Treatment of rats post SCI with genistein and CS/PVA nanofibers improved most of the above mentioned biochemical parameters and shifted them toward the control group values. Genistein induced an increase in the activity of SOD and the level of IL-10, while causing a decrease in the levels of NO, MDA and TNF-α in injured spinal cord tissue. Genistein and CS/PVA nanofibers provide a novel combination for treating inflammatory nervous tissue conditions, especially when combined as an implantable drug-delivery system.


2020 ◽  
Vol 34 (5) ◽  
pp. 6984-6998
Author(s):  
Ningning Chen ◽  
Pengxiang Zhou ◽  
Xizhe Liu ◽  
Jiachun Li ◽  
Yong Wan ◽  
...  

Oncogene ◽  
2002 ◽  
Vol 21 (34) ◽  
pp. 5255-5267 ◽  
Author(s):  
Yi Tang ◽  
Varalakshmi Katuri ◽  
Sohail Iqbal ◽  
Tina Narayan ◽  
Zhili Wang ◽  
...  

JAMA ◽  
1980 ◽  
Vol 244 (22) ◽  
pp. 2555-2555
Author(s):  
E. A. Neale

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1582 ◽  
Author(s):  
Takehiro Sugaya ◽  
Haruo Kanno ◽  
Michiharu Matsuda ◽  
Kyoichi Handa ◽  
Satoshi Tateda ◽  
...  

The receptor-interacting protein kinase 3 (RIPK3) is a key regulator of necroptosis and is involved in various pathologies of human diseases. We previously reported that RIPK3 expression is upregulated in various neural cells at the lesions and necroptosis contributed to secondary neural tissue damage after spinal cord injury (SCI). Interestingly, recent studies have shown that the B-RAFV600E inhibitor dabrafenib has a function to selectively inhibit RIPK3 and prevents necroptosis in various disease models. In the present study, using a mouse model of thoracic spinal cord contusion injury, we demonstrate that dabrafenib administration in the acute phase significantly inhibites RIPK3-mediated necroptosis in the injured spinal cord. The administration of dabrafenib attenuated secondary neural tissue damage, such as demyelination, neuronal loss, and axonal damage, following SCI. Importantly, the neuroprotective effect of dabrafenib dramatically improved the recovery of locomotor and sensory functions after SCI. Furthermore, the electrophysiological assessment of the injured spinal cord objectively confirmed that the functional recovery was enhanced by dabrafenib. These findings suggest that the B-RAFV600E inhibitor dabrafenib attenuates RIPK3-mediated necroptosis to provide a neuroprotective effect and promotes functional recovery after SCI. The administration of dabrafenib may be a novel therapeutic strategy for treating patients with SCI in the future.


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