scholarly journals Autophagy Activation Is Involved in Acidic Fibroblast Growth Factor Ameliorating Parkinson’s Disease via Regulating Tribbles Homologue 3

2019 ◽  
Vol 10 ◽  
Author(s):  
Xingfeng Zhong ◽  
Beini Wang ◽  
Guanyinsheng Zhang ◽  
Yuan Yuan ◽  
Xiaoli Hu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Acidic Fibroblast Growth Factor

Basic fibroblast growth factor increases dopaminergic graft survival and function in a rat model of Parkinson's disease

1995 ◽  
Vol 1 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Hldeichi Takayama ◽  
Jasodhara Ray ◽  
Heather K. Raymon ◽  
Andrew Baird ◽  
Joanna Hogg ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Graft Survival ◽  
Basic Fibroblast Growth Factor ◽  
Rat Model ◽  
Fibroblast Growth ◽  
And Function

scholarly journals Therapeutic effect of TO901317 on 6-OHDA-induced Parkinson rats in vitro and in vivo

2020 ◽  
Author(s):  
Miaomiao Li ◽  
Junqing Yang ◽  
Oumei Cheng ◽  
Zhe Peng ◽  
Yin Luo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Stem Cells ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Dopamine Neurons ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8

Abstract Background: Stem cells from different sources could differentiate into dopamine-producing cells and ameliorate behavioral deficits in Parkinsonian models. Especially, human bone marrow mesenchymal stem cells (hBMSCs) have many advantages without ethical dispute. Liver X receptor s (LXRs) are involved in the maintenance of the normal function of the central nervous system myelin. We have reported the induction of cocktail-induced da phenotypes from adult rat BMSCs by using sonic hedgehog (SHH), fibroblast growth factor 8 (FGF8), basic fibroblast growth factor (bFGF) and TO901317 (agonist of LXRs) with 87.42% of efficiency in 6 days of period of induction. But the previous work did not verify whether the induced cells had the corresponding neural function. Methods: In this study, we demonstrated that TO901317 could promote the differentiation of hBMSCs into dopaminergic neurons. Neuronal markers (Tuj1, Neun and Nestin), dopamine neuron markers (tyrosine hydroxylase, TH), LXRa and LXRb were detected by immunofluorescence. RT-qPCR was used to measure the mRNA expressions of adenosine triphosphate-binding cassette transporter A1 (ABCA1). Western Blotting detected the changes of LXRa, LXRb and TH expression. Results: TO901317 significantly enhanced the differentiation from hBMSCs to DA neurons. Only the LXR+GF group released dopamine by the result of enzyme linked immunosorbent assay (ELISA). Compared with the control group and GF group, the optimal time for differentiation of hBMSCs treated by 0.5mM TO901317 combined with GF was six days. And the maximum induction efficiency was 91.67%. After transplanting induced-cells into Parkinson's disease rats, the symptoms of Parkinson's rats decreased, and the number of dopamine neurons increased in the substantia nigra and striatum. Conclusions: TO901317 promoted differentiation of hBMSCs into dopamine neurons may be related to activation of LXR-ABCA1 signaling pathway. These data suggest that TO901317 may serve as a potential therapeutic methods for Parkinson's disease.

scholarly journals The Effect of MSCs Derived from the Human Umbilical Cord Transduced by Fibroblast Growth Factor-20 on Parkinson’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Li Jinfeng ◽  
Wang Yunliang ◽  
Liu Xinshan ◽  
Wang Shanshan ◽  
Xu Chunyang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Cell Therapy ◽  
Fibroblast Growth Factor ◽  
Umbilical Cord ◽  
Human Umbilical Cord ◽  
Fibroblast Growth ◽  
Mice Model ◽  
Factor 20

Cell therapy is a potential therapeutic approach for Parkinson’s disease (PD). Mesenchymal stem cells derived from the human umbilical cord (hUC-MSCs) give priority to PD patients because of multiple advantages. The appropriate gene transduction of hUC-MSC before transplantation is a promising procedure for cell therapy. Fibroblast growth factor-20 (FGF-20) has been shown to protect dopaminergic neurons against a range of toxic insults in vitro. In this study, the hUC-MSCs were gene transduced with FGF-20, and then we transplanted them into the PD mice model. The results showed that MSC-FGF-20 treatment obviously improved the behavior of PD, accompanied by the increase of tyrosine carboxylase- (TH-) positive cell and dopamine (DA). Furtherly, immunohistochemistry disclosed that MSC-FGF-20 obviously promoted the degradation of nuclear factor-κB (NF-κB), a transcription factor that controls genes encoding proinflammatory cytokines, highly expressed in the nigrostriatal dopaminergic regions in PD patients. Therefore, MSC-FGF-20 has a potential for improving PD, closely related to the degradation of NF-κB.

Loss of basic fibroblast growth factor in substantia nigra neurons in Parkinson's disease

Neurology ◽  
1993 ◽  
Vol 43 (2) ◽  
pp. 372-372 ◽  
Author(s):  
I. Tooyama ◽  
T. Kawamata ◽  
D. Walker ◽  
T. Yamada ◽  
K. Hanai ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Substantia Nigra ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth

Canopy Fibroblast Growth Factor Signaling Regulator 2 (CNPY2) Inhibits Neuron Apoptosis in Parkinson’s Disease via AKT/GSK3β pathway

2021 ◽  
Vol 18 ◽  
Author(s):  
Miao Chu ◽  
Huimiao Liu ◽  
Zhaohui Xiong ◽  
Chaojuan Ju ◽  
Lina Zhao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Signaling Pathway ◽  
Growth Factor Signaling ◽  
Fibroblast Growth ◽  
Mitochondria Dysfunction ◽  
Fibroblast Growth Factor Signaling

Background: Parkinson’s disease (PD) is a neurodegenerative disorder caused by the progressive loss of dopaminergic neurons. Canopy fibroblast growth factor signaling regulator 2 (CNPY2) is down-regulated in this disease, but its functions are unknown. Objective: This study investigates the effects and regulation of CNPY2 in the apoptosis of neurons in PD. Methods: We established a PD model in vivo by a five consecutive days-injection of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) to mice. In vitro, the human SH-SY5Y neuroblastoma cells, after differentiation, were treated with 1-Methyl-4-phenylpyridinium iodide (MPP+) for modeling. The cells were transfected with a recombinant vector overexpressing CNPY2 followed by MPP+ treatment. Expression of CNPY2 and proteins related to apoptosis was detected by real-time PCR, western blot, or immunofluorescence staining. The ROS level and mitochondrial membrane potential were determined by flow cytometry. Cell viability and apoptosis were measured by MTT assay and TUNEL staining. Results: CNPY2 level was down-regulated both in the brain and retina of PD mice and also inhibited in neurons by MPP+ in vitro. Overexpression of CNPY2 repressed the level of Bax and cleaved caspase-3, enhanced Bcl-2 level, and promoted neurite length under MPP+ treatment. CNPY2 overexpression reduced the accumulation of ROS and mitochondria dysfunction in neurons. The AKT/GSK3β signaling pathway was activated by overexpressed CNPY2 to inhibit MPP+-induced neuronal apoptosis, which was confirmed using an AKT inhibitor MK-2206 2HCl. Conclusion: CNPY2 alleviates oxidative stress, mitochondria dysfunction, and apoptosis of neurons induced by MPP+ by activating the AKT/ GSK3β signaling pathway

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