Human Amniotic Epithelial Cells Alleviate a Mouse Model of Parkinson’s Disease Mainly by Neuroprotective, Anti-Oxidative and Anti-Inflammatory Factors

2020 ◽  
Author(s):  
Jiaofei Zhang ◽  
Hui Li ◽  
Hao Yang ◽  
Jianhua Lin ◽  
You Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Inflammatory Factors ◽  
Amniotic Epithelial Cells ◽  
Human Amniotic Epithelial Cells ◽  
Anti Inflammatory

scholarly journals Human Amniotic Epithelial Cells Recover Mouse model of Parkinson’s Disease mainly by Neuroprotective，Anti-oxidative and Anti-inflammatory factors

2020 ◽  
Author(s):  
Jiaofei Zhang ◽  
Hui Li ◽  
Hao Yang ◽  
Jianhua Lin ◽  
You Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Inflammatory Factors ◽  
Amniotic Epithelial Cells ◽  
Human Amniotic Epithelial Cells ◽  
Anti Inflammatory

Abstract The authors have withdrawn this preprint due to author disagreement.

scholarly journals Hyaluronic acid ameliorates the proliferative ability of human amniotic epithelial cells through activation of TGF-β/BMP signaling

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10104
Author(s):  
Ya-Bing Tian ◽  
Nuo-Xin Wang ◽  
Yan Xu ◽  
Chang-Yin Yu ◽  
Ru-Ming Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hyaluronic Acid ◽  
Epithelial Cells ◽  
Bmp Signaling ◽  
Inflammatory Factors ◽  
Proliferative Effect ◽  
Amniotic Epithelial Cells ◽  
Human Amniotic Epithelial Cells ◽  
Proliferative Ability

Human amniotic epithelial cells (hAECs) are a useful and noncontroversial source of stem cells for cell therapy and regenerative medicine, but their limited proliferative ability hinders the acquisition of adequate quantities of cells for clinical use due to not expressing telomerase in hAECs. Our previous study showed that hyaluronic acid (HA), an important component of the extracellular matrix, promoted the proliferation of human amniotic mesenchymal stem cells. Herein, we hypothesize that HA might improve the proliferative capability of hAECs. In the present study, the role of HA on the proliferation of human amniotic epithelial cells (hAECs) in vitro was investigated for the first time. HA at molecular weight of 300 kDa showed an obvious pro-proliferation effect on hAECs. Furthermore, HA not only kept phenotypic characteristics and differentiation capabilities of hAECs, but significantly promoted the secretion of the anti-inflammatory factors such as IL-10 and TGF-β1, and the expression of stem cell pluripotent factors such as Oct4 and Nanog. Analysis of PCR microarray data and RT-qPCR validation showed that TGF-β/BMP signaling was activated in the presence of HA. Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling, significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B, SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs. These data suggest that HA is a safe and effective enhancer for in vitro expansion of hAECs, whose regulatory mechanism involves the TGF-β/BMP signaling.

Catalpol Exerts Neuroprotective Effect on 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-Induced Mouse Model of Parkinson’s Disease and the Underlying Mechanisms

2021 ◽  
Vol 11 (8) ◽  
pp. 1506-1516
Author(s):  
Xueqian Li ◽  
Chengzhi Zhao
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Performance Test ◽  
Behavioral Science ◽  
Neuroprotective Effect ◽  
Inflammatory Factors ◽  
Sod Activity ◽  
Novel Approach ◽  
Underlying Mechanisms

Our current study aimed to assess the preventive and therapeutic impacts of catalpol on Parkinson’s disease (PD) and its possible mechanism. In this study, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were employed to establish a PD model and then treated with catalpol followed by analysis of behavioral science by open field test, pole-climbing assay and rotarod performance test, ROS and SOD activity and expression of TH, DAT, VEGF and GAP43 by western blot or immunofluorescence. The results disclosed that catalpol can ameliorate the MPTP-triggered loss of dopamine (DA)-producing neurons, while it was able to enhance the expression of tyrosine hydroxylase (TH), accompanied by the activation of astrocytes and microglia. Catalpol treatment significantly retarded the oxidative stress induced by MPTP, along with elevated levels of VEGF and growth-associated protein 4 (GAP43). Additionally, catalpol treatment activated the MKK4/JNK/c-Jun signal pathway in PD mouse model, accompanied by reduced secretion of pro-inflammatory factors. Catalpol executed the anti-apoptotic and anti-oxidant impacts on MPTP-induced Parkinson’s model, suggesting that it might be a novel approach for treating PD in the future.

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