Co‑culturing with hypoxia pre‑conditioned mesenchymal stem cells as a new strategy for the prevention of irradiation‑induced fibroblast‑to‑myofibroblast transition

Zhuang, Lei; Xia, Wenzheng; Hou, Meng

doi:10.3892/or.2019.7293

Cited by 7 publications

(6 citation statements)

References 46 publications

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“…Western Blot analysis was conducted as previously described [ 49 ]. Primary antibodies, including p27 kip (ab62364), p16 INK4a (ab211542), Flotillin-1 (ab41927), CD81 (ab109201), Sirt2 (ab211033), and β-actin (ab179467), were purchased from Abcam.…”

Section: Methodsmentioning

confidence: 99%

Exosomal LncRNA–NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p

et al. 2020

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Background The chemotherapy drug doxorubicin (Dox) is widely used for treating a variety of cancers. However, its high cardiotoxicity hampered its clinical use. Exosomes derived from stem cells showed a therapeutic effect against Dox-induced cardiomyopathy (DIC). Previous studies reported that exosomes derived from mesenchymal stem cells (MSCs) pretreated with macrophage migration inhibitory factor (MIF) (exosomeMIF) showed a cardioprotective effect through modulating long noncoding RNAs/microRNAs (lncRNAs/miRs). This study aimed to investigate the role of exosomeMIF in the treatment of DIC. Results Exosomes were isolated from control MSCs (exosome) and MIF-pretreated MSCs (exosomeMIF). Regulatory lncRNAs activated by MIF pretreatment were explored using genomics approaches. Fluorescence-labeled exosomes were tracked in vitro by fluorescence imaging. In vivo and in vitro, miR-221-3p mimic transfection enforced miR-221-3p overexpression, and senescence-associated β-galactosidase assay was applied to test cellular senescence. Exosomal delivering LncRNA-NEAT1 induced therapeutic effect in vivo was confirmed by echocardiography. It demonstrated that exosomesMIF recovered the cardiac function and exerted the anti-senescent effect through LncRNA–NEAT1 transfer against Dox. TargetScan and luciferase assay showed that miR-221-3p targeted the Sirt2 3′-untranslated region. Silencing LncRNA–NEAT1 in MSCs, miR-221-3p overexpression or Sirt2 silencing in cardiomyocytes decreased the exosomeMIF-induced anti-senescent effect against Dox. Conclusions The results indicated exosomeMIF serving as a promising anti-senescent effector against Dox-induced cardiotoxicity through LncRNA–NEAT1 transfer, thus inhibiting miR-221-3p and leading to Sirt2 activation. The study proposed that exosomeMIF might have the potential to serve as a cardioprotective therapeutic agent during cancer chemotherapy.

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Section: Methodsmentioning

confidence: 99%

Exosomal LncRNA–NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p

et al. 2020

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“…Hypoxic mesenchymal stem cells, upon implantation, had a reversal on cardiac fibrosis via prevention of fibroblast to myofibroblast transition [34].…”

Section: Hypoxiamentioning

confidence: 99%

Cardiac Stem Cell Therapy, Resident Progenitor Cells and the role of Cellular Signalling; a Review

Hutchings

Nawrocki

Mozdziak

et al. 2019

Medical Journal of Cell Biology

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Cardiovascular disease (CVD) remains the most common cause of death worldwide. Unhealthy lifestyle choices promote an upward trend of primary risk factors for CVD. As a result, novel methods of treatment are required. The myocardium itself could serve as a source of treatment, via resident cardiac progenitor cells (CPC). A brief overview of current studies and findings related to the potential of differentiation of CPCs to form mature cardiomyocytes (CM) and thereby heal damaged myocardial tissue, as well as implications of these findings for further research areas and possible treatments, is offered. Also investigated is the possible role of CM cell reprogramming, cardiac fibroblasts and signalling molecules in treatment of CVD. Running title: Cardiac stem cells -review

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“…Other studies have shown that fibroblasts are targets of MSC, demonstrating an interplay between the two. Conditioned media from and cocultures with MSC have been shown to suppress the proliferation and myofibroblast differentiation of fibroblasts (155,157,160). Everything considered, while necessary and informative, in vitro work must always be taken with a grain of salt as not all culture conditions are physiologically relevant or reproducible in vivo, and culture conditions can even make a cancer cell appear phenotypically normal (152).…”

Section: Limitations and Current Needs In The Fieldmentioning

confidence: 99%

Lung-resident mesenchymal stromal cells are tissue-specific regulators of lung homeostasis

Sveiven

Nordgren

2020

American Journal of Physiology-Lung Cellular and Molecular Phys

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Until recently, data supporting the tissue-resident status of mesenchymal stromal cells (MSC) has been ambiguous since their discovery in the 1950–60s. These progenitor cells were first discovered as bone marrow-derived adult multipotent cells and believed to migrate to sites of injury, opposing the notion that they are residents of all tissue types. In recent years, however, it has been demonstrated that MSC can be found in all tissues and MSC from different tissues represent distinct populations with differential protein expression unique to each tissue type. Importantly, these cells are efficient mediators of tissue repair, regeneration, and prove to be targets for therapeutics, demonstrated by clinical trials ( phase 1– 4) for MSC-derived therapies for diseases like graft-versus-host-disease, multiple sclerosis, rheumatoid arthritis, and Crohn’s disease. The tissue-resident status of MSC found in the lung is a key feature of their importance in the context of disease and injuries of the respiratory system, since these cells could be instrumental to providing more specific and targeted therapies. Currently, bone marrow-derived MSC have been established in the treatment of disease, including diseases of the lung. However, with lung-resident MSC representing a unique population with a different phenotypic and gene expression pattern than MSC derived from other tissues, their role in remediating lung inflammation and injury could provide enhanced efficacy over bone marrow-derived MSC methods. Through this review, lung-resident MSC will be characterized, using previously published data, by surface markers, gene expression patterns, and compared with bone-marrow MSC to highlight similarities and, importantly, differences in these cell types.

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Co‑culturing with hypoxia pre‑conditioned mesenchymal stem cells as a new strategy for the prevention of irradiation‑induced fibroblast‑to‑myofibroblast transition

Cited by 7 publications

References 46 publications

Exosomal LncRNA–NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p

Exosomal LncRNA–NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p

Cardiac Stem Cell Therapy, Resident Progenitor Cells and the role of Cellular Signalling; a Review

Lung-resident mesenchymal stromal cells are tissue-specific regulators of lung homeostasis

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