Bone marrow mesenchymal stem cells‐derived conditioned medium protects cardiomyocytes from hypoxia/reoxygenation‐induced injury through Notch2/mTOR/autophagy signaling

2019 ◽  
Vol 234 (10) ◽  
pp. 18906-18916 ◽  
Author(s):  
Xianyu Li ◽  
Xiaolin Xie ◽  
Zhui Yu ◽  
Yun Chen ◽  
Gaojing Qu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Conditioned Medium ◽  
Marrow Mesenchymal Stem Cells ◽  
Hypoxia Reoxygenation

Conditioned medium enhances the fusion capability of rat bone marrow mesenchymal stem cells and cardiomyocytes

2014 ◽  
Vol 41 (5) ◽  
pp. 3099-3112 ◽  
Author(s):  
Kanwal Haneef ◽  
Nadia Naeem ◽  
Irfan Khan ◽  
Hana’a Iqbal ◽  
Nurul Kabir ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Conditioned Medium ◽  
Marrow Mesenchymal Stem Cells ◽  
Rat Bone

scholarly journals Differentiation of Bone Marrow Mesenchymal Stem Cells into Neural Lineage Cells Induced by bFGF-Chitosan Controlled Release System

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Manli Li ◽  
Wen Zhao ◽  
Yudan Gao ◽  
Peng Hao ◽  
Junkui Shang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Controlled Release ◽  
Conditioned Medium ◽  
Serum Starvation ◽  
Neural Lineage ◽  
Release System ◽  
Marrow Mesenchymal Stem Cells ◽  
Controlled Release System

Bone marrow mesenchymal stem cells undergo differentiation to different lineages with different efficiencies when induced by different factors. We added a bFGF-chitosan controlled release system (bFGF-CCRS) as an inducer into conditioned medium to facilitate the oriented differentiation of BMSCs into neural lineage cells (eventually mature neurons); furthermore, we synchronized BMSCs to the G0/G1 phase via serum starvation to observe the effect of the inducer on the differentiation direction and efficiency. The nonsynchronized group, chitosan alone (not loaded with bFGF) group, soluble bFGF group, and conditioned medium group served as controls, and we observed the dynamic process of differentiation of BMSCs into neural lineage cells at different time points after the beginning of coculture. We analyzed the binding patterns of bFGF and chitosan and assayed the expression differences of key factors (FGFR1, ERK, and c-fos) and molecular switches (BTG2) that regulate the transformation from cell proliferation to differentiation. We also investigated the potential molecular mechanism of BMSC differentiation into neural lineage cells at a high percentage when induced by bFGF-CCRS.

Mir-36a Inhibits Hypoxia Reoxygenation and Promotes Bone Marrow Mesenchymal Stem Cells to Promote Cardiomyocyte Repair

2021 ◽  
Vol 11 (12) ◽  
pp. 2491-2496
Author(s):  
Zhiting Sun ◽  
Kangni Yang ◽  
Hongyun Zhao
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Myocardial Injury ◽  
Myocardial Damage ◽  
Expression Of Genes ◽  
Damage Repair ◽  
Marrow Mesenchymal Stem Cells ◽  
Specific Mrnas ◽  
Hypoxia Reoxygenation

This study explores the mechanism of miR-36a in the hypoxia-reoxygenation process and its engagement in the repair of cardiomyocytes via modulating bone marrow mesenchymal stem cells (BMSCs). Thirty-two patients with myocardial injury were enrolled after hospitalization. Meanwhile, 32 normal patients were recruited as controls. The miR-36a levels were quantified via ELISA. BMSCs were isolated and cultured. The qRT-PCR was employed to determine the expression of genes involved in myocardial injury and hypoxia-reoxygenation, including KGF, SpB, SpA, CK18, SpC and Occludin. Specific mRNAs related to myocardial damage repair were also measured after miR-36a was knockdown and overexpressed during the process of repair induction. The expression of miR-36a in 32 patients with myocardial injury was elevated compared to that in controls. BMSCs can quantitatively retard the expression of hypoxia-reoxygenation-related genes. The knockdown of miR-36a can significantly enhance the expression of hypoxia-reoxygenation-related genes which were engaged in myocardial injury. miR-36a overexpression can significantly impede the expression of the hypoxia-reoxygenation-related genes which were involved in myocardial injury. miR-36a contributes to the repair of myocardial injury via functionally enhancing BMSCs’ function and interfering with the hypoxia-reoxygenation process.

scholarly journals Attenuating Spinal Cord Injury by Conditioned Medium from Bone Marrow Mesenchymal Stem Cells

2018 ◽  
Vol 8 (1) ◽  
pp. 23 ◽  
Author(s):  
May-Jywan Tsai ◽  
Dann-Ying Liou ◽  
Yan-Ru Lin ◽  
Ching-Feng Weng ◽  
Ming-Chao Huang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Bone Marrow ◽  
Spinal Cord Injury ◽  
Mesenchymal Stem Cells ◽  
Conditioned Medium ◽  
Cell Based Therapy ◽  
Cord Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
Related Proteins

Spinal cord injury (SCI) is a devastating neurological condition and might even result in death. However, current treatments are not sufficient to repair such damage. Bone marrow mesenchymal stem cells (BM-MSC) are ideal transplantable cells which have been shown to modulate the injury cascade of SCI mostly through paracrine effects. The present study investigates whether systemic administration of conditioned medium from MSCs (MSCcm) has the potential to be efficacious as an alternative to cell-based therapy for SCI. In neuron-glial cultures, MSC coculture effectively promoted neuronal connection and reduced oxygen glucose deprivation-induced cell damage. The protection was elicited even if neuron-glial culture was used to expose MSCcm, suggesting the effects possibly from released fractions of MSC. In vivo, intravenous administration of MSCcm to SCI rats significantly improved behavioral recovery from spinal cord injury, and there were increased densities of axons in the lesion site of MSCcm-treated rats compared to SCI rats. At early days postinjury, MSCcm treatment upregulated the protein levels of Olig 2 and HSP70 and also increased autophage-related proteins in the injured spinal cords. Together, these findings suggest that MSCcm treatment promotes spinal cord repair and functional recovery, possibly via activation of autophagy and enhancement of survival-related proteins.

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