Human Neural Stem Cell-Conditioned Medium Inhibits Inflammation in Macrophages Via Sirt-1 Signaling Pathway In Vitro and Promotes Sciatic Nerve Injury Recovery in Rats

2020 ◽  
Vol 29 (16) ◽  
pp. 1084-1095
Author(s):  
Tianyan Chen ◽  
Yilei Li ◽  
Wei Ni ◽  
Bin Tang ◽  
Yusheng Wei ◽  
...  
Keyword(s):  
Stem Cell ◽  
Sciatic Nerve ◽  
Conditioned Medium ◽  
Signaling Pathway ◽  
Nerve Injury ◽  
Neural Stem Cell ◽  
Human Neural Stem Cell ◽  
Injury Recovery ◽  
Cell Conditioned Medium

Therapeutic mechanism of human neural stem cell-derived extracellular vesicles against hypoxia-reperfusion injury in vitro

Life Sciences ◽  
2020 ◽  
Vol 254 ◽  
pp. 117772 ◽  
Author(s):  
Qingyue Liu ◽  
Yi Tan ◽  
Tingyu Qu ◽  
Jianhui Zhang ◽  
Xuexia Duan ◽  
...  
Keyword(s):  
Stem Cell ◽  
Reperfusion Injury ◽  
Neural Stem Cell ◽  
Extracellular Vesicles ◽  
Human Neural Stem Cell ◽  
Therapeutic Mechanism

scholarly journals The Potential of a Hair Follicle Mesenchymal Stem Cell-Conditioned Medium for Wound Healing and Hair Follicle Regeneration

2020 ◽  
Vol 10 (8) ◽  
pp. 2646
Author(s):  
Keng-Liang Ou ◽  
Yun-Wen Kuo ◽  
Chia-Yu Wu ◽  
Bai-Hung Huang ◽  
Fang-Tzu Pai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Hair Follicle ◽  
Conditioned Medium ◽  
Hair Growth ◽  
Hair Regeneration ◽  
Hacat Keratinocyte ◽  
Cell Conditioned Medium

The study elucidated the wound healing and hair regeneration properties of a conditioned medium prepared from the culture of human hair follicle mesenchymal stem cells (HFMSCs). The wound-healing effects of mesenchymal stem cell-conditioned medium (MSC-CM) were tested in vitro using scratch assays co-cultured with HaCaT keratinocyte and monitored through optical microscopy. The cell proliferation of HFMSCs and the HaCaT keratinocyte were observed in the presence of different kinds of drugs including UK5099, sodium L-lactate, lactate dehydrogenase-A, MSC-CM, caffeine, and caffeic acid. The hair regeneration properties were investigated in vivo by administrating the MSC-CM solutions to adult B6 mouse models. For quantification, hematoxylin and eosin staining were performed following euthanasia. In vitro results revealed that MSC-CM promotes dermal cell migrations and enhances proliferation of HFMSCs and HaCaT keratinocytes, demonstrating wound-healing properties. Moreover, when the MSC-CM solutions were applied to the shaved mouse skin, a dark area that expanded overtime was seen. Although no hair growth was found, histological analysis proved that a fat layer thickness increment was found under the mouse’s skin, ultimately projecting the formation of new hair growth. MSC-CM promotes the migration and proliferation of dermal keratinocytes that are beneficial for wound healing and hair growth. It is believed that MSC-CM can potentially serve as the basis of alternative therapeutic applications for wound closure and skin regeneration as well as hair growth stimulation and hair loss prevention in alopecia.

scholarly journals Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway

2020 ◽  
Author(s):  
Guoyong Jia ◽  
Hongna Yang ◽  
Zengyan Diao ◽  
Ying Liu ◽  
Congcong Sun
Keyword(s):  
Stem Cell ◽  
Cell Viability ◽  
Conditioned Medium ◽  
Neural Stem Cell ◽  
Inhibitory Effect ◽  
Complete Medium ◽  
Dependent Manner ◽  
Induced Apoptosis ◽  
Dose Dependent ◽  
Cell Conditioned Medium

Alzheimer’s disease (AD) is a progressive, neurodegenerative disease. Accumulating evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue (substantia nigra, blue plaque, paraventricular nucleus). In this study, we investigated the effect of neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβ25-35 significantly decreased the cell viability in time and dose dependent manner. However, Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had inhibitory effect on toxicity when fibrillation of Aβ25-35 occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβ25-35 + NSC-CDM group. sh-PCMT1 significantly reduced the PCMT1, the cell viability and inhibited the protective effect; induced apoptosis and increased the expression of p-MST1. Overexpression of PCMT1 group reversed the effect of Aβ25-35 inhibited the cell viability and Aβ25-35 induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβ25-35 to cells by increasing PCMT1, reducing MST phosphorylation.

scholarly journals BDNF promotes human neural stem cell growth via GSK-3β-mediated crosstalk with the wnt/β-catenin signaling pathway

2016 ◽  
Vol 34 (1-2) ◽  
pp. 19-32 ◽  
Author(s):  
Jin-Wei Yang ◽  
Wei Ma ◽  
Tao Luo ◽  
Dong-Yan Wang ◽  
Jian-Jun Lu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Neural Stem Cell ◽  
Human Neural Stem Cell ◽  
Gsk 3Β

scholarly journals Neural stem cell-conditioned medium ameliorates Aβ25–35-induced damage in SH-SY5Y cells by protecting mitochondrial function

2020 ◽  
Author(s):  
Guoyong Jia ◽  
Zengyan Diao ◽  
Ying Liu ◽  
Congcong Sun ◽  
Cuilan Wang
Keyword(s):  
Stem Cell ◽  
Cytochrome C ◽  
Cell Viability ◽  
Conditioned Medium ◽  
Neural Stem Cell ◽  
Mitochondrial Morphology ◽  
Complete Medium ◽  
Ros Production ◽  
Expression Levels ◽  
Cell Conditioned Medium

Inhibition of amyloid β (Aβ)-induced mitochondrial damage is considered crucial for reducing the pathological damage in Alzheimer’s disease (AD). We evaluated the effect of neural stem cell-conditioned medium (NSC-CDM) on Aβ25–35-induced damage in SH-SY5Y cells. An in vitro model of AD was established by treating SH-SY5Y cells with 40 μM Aβ25–35 for 24 h. SH-SY5Y cells were divided into control, Aβ25–35 (40 μM), Aβ25–35 (40 μM) + NSC-CDM, and Aβ25–35 (40 μM) + neural stem cell-complete medium (NSC-CPM) groups. Cell viability was detected by CCK-8 assay. Apoptosis, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) were detected by flow cytometry. Malondialdehyde (MDA) content was detected by ELISA assay. Western blot analysis was used to detect cytochrome c release and apoptosis-related proteins. Transmission electron microscopy (TEM) was used to observe mitochondrial morphology. Cell viability significantly decreased and apoptosis significantly increased in SH-SY5Y cells treated with Aβ25–35, and both effects were rescued by NSC-CDM. In addition, NSC-CDM reduced ROS production and significantly inhibited the reduction of MMP caused by Aβ25–35. Furthermore, NSC-CDM ameliorated Aβ25–35-induced reduction in Bcl-2 expression levels and increased the expression levels of cytochrome c, caspase-9, caspase-3, and Bax. Moreover, Aβ25–35 induced the destruction of mitochondrial ultrastructure and this effect was reversed by NSC-CDM. Collectively, our findings demonstrated the protective effect of NCS-CDM against Aβ25–35-induced SH-SY5Y cell damage and clarified the mechanism of action of Aβ25–35 in terms of mitochondrial maintenance and mitochondria-associated apoptosis signaling pathways, thus providing a theoretical basis for the development of novel anti-AD treatments.

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