Designed cyclopentenone prostaglandin derivatives as neurite outgrowth-promoting compounds for CAD cells, a rat catecholaminergic neuronal cell line of the central nervous system

2000 ◽  
Vol 291 (3) ◽  
pp. 167-170 ◽  
Author(s):  
Takumi Satoh ◽  
Kyoji Furuta ◽  
Keiichiro Tomokiyo ◽  
Masaaki Suzuki ◽  
Yasuyoshi Watanabe

2002 ◽  
Vol 67 (5) ◽  
pp. 1908-1920 ◽  
Author(s):  
Eva M. Eves ◽  
Lawrence H. Boise ◽  
Craig B. Thompson ◽  
Andrew J. Wagner ◽  
Nissim Hay ◽  
...  


1994 ◽  
Vol 269 (45) ◽  
pp. 28181-28186
Author(s):  
A M Ho ◽  
J Jain ◽  
A Rao ◽  
P G Hogan


Author(s):  
Marleen H. van Coevorden-Hameete ◽  
Maarten J. Titulaer ◽  
Marco W. J. Schreurs ◽  
Esther de Graaff ◽  
Peter A. E. Sillevis Smitt ◽  
...  


Neuron ◽  
1994 ◽  
Vol 13 (3) ◽  
pp. 541-554 ◽  
Author(s):  
Barry G. Condron ◽  
Nipam H. Patel ◽  
Kai Zinn


2000 ◽  
Vol 28 (4) ◽  
pp. 452-455 ◽  
Author(s):  
D. E. Brenneman ◽  
C. Y. Spong ◽  
I. Gozes

In studying the mediators of VIP neurotrophism in the central nervous system, two glial proteins have been discovered. Both of these proteins contain short peptides that exhibit femtomolar potency in preventing neuronal cell death from a wide variety of neurotoxic substances. Extension of these peptides to models of oxidative stress or neurodegeneration in vivo have indicated significant efficacy in protection. These peptides, both as individual agents and in combination, have promise as possible protective agents in the treatment of human neurodegenerative disease and in pathologies involving oxidative stress.



2021 ◽  
Vol 15 ◽  
Author(s):  
Yongliang Wang ◽  
Ruxia Han ◽  
Zhejun Xu ◽  
Xiahui Sun ◽  
Chunxue Zhou ◽  
...  

Toxoplasma gondii is neurotropic and affects the function of nerve cells, while the mechanism is unclear. LncRNAs are abundantly enriched in the brain and participated in the delicate regulation of the central nervous system (CNS) development. However, whether these lncRNAs are involved in the regulation of microglia activation during the process of T. gondii infection is largely unknown. In this study, the upregulation of a novel lncRNA147410.3 (ENSMUST00000147410.3) was identified as a key factor to influence this process. The target gene of lncRNA147410.3 was predicted and identified as Hoxb3. The localization of lncRNA147410.3 in the brain and cells was proved in the nucleus of neuroglia through FISH assay. Furthermore, the function of lncRNA147410.3 on neuronal cell was confirmed that lncRNA147410.3 could affect proliferation, differentiation, and apoptosis of mouse microglia by positively regulating Hoxb3. Thus, our study explored the modulatory action of lncRNA147410.3 in T. gondii infected mouse brain, providing a scientific basis for using lncRNA147410.3 as a therapeutic target to treat neurological disorder induced by T. gondii.



Vaccines ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 485 ◽  
Author(s):  
Sarah Stonedahl ◽  
Penny Clarke ◽  
Kenneth L. Tyler

Encephalitis resulting from viral infections is a major cause of hospitalization and death worldwide. West Nile Virus (WNV) is a substantial health concern as it is one of the leading causes of viral encephalitis in the United States today. WNV infiltrates the central nervous system (CNS), where it directly infects neurons and induces neuronal cell death, in part, via activation of caspase 3-mediated apoptosis. WNV infection also induces neuroinflammation characterized by activation of innate immune cells, including microglia and astrocytes, production of inflammatory cytokines, breakdown of the blood-brain barrier, and infiltration of peripheral leukocytes. Microglia are the resident immune cells of the brain and monitor the CNS for signs of injury or pathogens. Following infection with WNV, microglia exhibit a change in morphology consistent with activation and are associated with increased expression of proinflammatory cytokines. Recent research has focused on deciphering the role of microglia during WNV encephalitis. Microglia play a protective role during infections by limiting viral growth and reducing mortality in mice. However, it also appears that activated microglia are triggered by T cells to mediate synaptic elimination at late times during infection, which may contribute to long-term neurological deficits following a neuroinvasive WNV infection. This review will discuss the important role of microglia in the pathogenesis of a neuroinvasive WNV infection. Knowledge of the precise role of microglia during a WNV infection may lead to a greater ability to treat and manage WNV encephalitis.



Sign in / Sign up

Export Citation Format

Share Document