MicroRNA-211 causes ganglion cell dysplasia in congenital intestinal atresia via down-regulation of glial-derived neurotrophic factor

2015 ◽  
Vol 28 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Z.-q. Xia ◽  
D.-k. Ding ◽  
N. Zhang ◽  
J.-x. Wang ◽  
H.-y. Yang ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Neurotrophic Factor ◽  
Intestinal Atresia ◽  
Down Regulation ◽  
Glial Derived Neurotrophic Factor

Poster #113 BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF), NEUROTROPHIN 3 (NTF3), NEUROTROPHIN 4 (NTF4) AND GLIAL-DERIVED NEUROTROPHIC FACTOR (GDNF) SERUM LEVELS IN SCHIZOPHRENIA

2012 ◽  
Vol 136 ◽  
pp. S132-S133
Author(s):  
Anna Leszczynska-Rodziewicz ◽  
Maria Skibinska ◽  
Pawel Kapelski ◽  
Aleksandra Rajewska-Rager ◽  
Joanna Pawlak ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Neurotrophin 3 ◽  
Glial Derived Neurotrophic Factor

scholarly journals Paracrine regulation of glioma cells invasion by astrocytes is mediated by glial-derived neurotrophic factor

2014 ◽  
Vol 137 (5) ◽  
pp. 1012-1020 ◽  
Author(s):  
Ayelet Shabtay-Orbach ◽  
Moran Amit ◽  
Yoav Binenbaum ◽  
Shorook Na'ara ◽  
Ziv Gil
Keyword(s):  
Neurotrophic Factor ◽  
Glioma Cells ◽  
Paracrine Regulation ◽  
Glial Derived Neurotrophic Factor

scholarly journals How Antidepressant Drugs Affect the Antielectroshock Action of Antiseizure Drugs in Mice: A Critical Review

2021 ◽  
Vol 22 (5) ◽  
pp. 2521
Author(s):  
Kinga K. Borowicz-Reutt
Keyword(s):  
Antiepileptic Drugs ◽  
Neurotrophic Factor ◽  
Antidepressant Drugs ◽  
Drug Effects ◽  
Mechanisms Of Action ◽  
Maximal Electroshock ◽  
Anticonvulsant Action ◽  
Mes Test ◽  
Seizure Model ◽  
Glial Derived Neurotrophic Factor

Depression coexists with epilepsy, worsening its course. Treatment of the two diseases enables the possibility of interactions between antidepressant and antiepileptic drugs. The aim of this review was to analyze such interactions in one animal seizure model—the maximal electroshock (MES) in mice. Although numerous antidepressants showed an anticonvulsant action, mianserin exhibited a proconvulsant effect against electroconvulsions. In most cases, antidepressants potentiated or remained ineffective in relation to the antielectroshock action of classical antiepileptic drugs. However, mianserin and trazodone reduced the action of valproate, phenytoin, and carbamazepine against the MES test. Antiseizure drug effects were potentiated by all groups of antidepressants independently of their mechanisms of action. Therefore, other factors, including brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) modulation, should be considered as the background for the effect of drug combinations.

Bone Marrow Stromal Cells (BMSCs) Inhibit Retinal Ganglion Cell Apoptosis and Alleviate Inflammation Through Up-Regulation of MicroRNA-43 and Brain-Derived Neurotrophic Factor in Glaucoma

2021 ◽  
Vol 11 (12) ◽  
pp. 2478-2483
Author(s):  
Xiang Ji ◽  
Kai-Wen Zhou
Keyword(s):  
Neurotrophic Factor ◽  
Vision Loss ◽  
Luciferase Reporter ◽  
Retinal Ganglion ◽  
Luciferase Reporter Gene ◽  
Down Regulation ◽  
Related Factors ◽  
Gene Assay

Glaucoma is a leading cause of vision loss mainly due to retinal ganglion cells (RGC) loss. MicroRNAs (miRNAs) are highlighted as potential biomarkers in diseases. This study aims to investigate the role of miR-43 and BMSCs in the RGC apoptosis and glaucoma.RGCs were transfected with miR-43 inhibitors and mimics, and then co-cultured with BMSCs. RT-qPCR analysis was conducted to determine miR-43 expression, whilst Western blot, and flow cytometry were carried out to assess the role of miR-43 in apoptosis and inflammation. The interaction between miR-43 and BDNF, a neurotrophic factor, was detected by dual-luciferase reporter gene assay. Overexpression of miR-43 promoted RGC proliferation and decreased apoptosis. Furthermore, miR-43 overexpression diminished the contents of apoptosis- and inflammatory-related factors, and elevated the expression of BDNF. Down-regulation of BDNF exerted similar effect as down-regulation of miR-43, enhancing apoptosis and aggravating inflammation. Importantly, BMSC treatment reversed the in vitro inhibitory effect of si-BDNF on RGC with enhancement of miR-43 expression. Mechanically, miR-43 was indicated to target BDNF in glaucoma. Collectively, miR-43 delivered by BMSCs plays an important role in the inflammatory injury and abnormal apoptosis of RGC by regulating the expression of BDNF. These findings might help development of new treatment for glaucoma and provide a promising biomarker for diagnosis and treatment.

Down-regulation of Glutamate-induced Conductances of Retinal Horizontal Cells After Ganglion Cell Axotomy

2002 ◽  
Vol 75 (2) ◽  
pp. 209-216 ◽  
Author(s):  
RomÁn Blanco ◽  
Francisco Germain ◽  
Almudena Velasco ◽  
Pedro de la Villa
Keyword(s):  
Ganglion Cell ◽  
Horizontal Cells ◽  
Down Regulation
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