Mesenchymal stem cells rescue injured endothelial cells in an in vitro ischemia–reperfusion model via tunneling nanotube like structure-mediated mitochondrial transfer

Liu, Kaiming; Ji, Kunqian; Guo, Liang; Wu, Wei; Lu, Huixia; Shan, Peiyan; Yan, Chuanzhu

doi:10.1016/j.mvr.2014.01.008

Cited by 292 publications

(276 citation statements)

References 43 publications

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“…A second plausible method of protection is that the BMSC binds to an injured intestinal cell and "downloads" vital materials into the native cell such as mitochondria, ATP, or other vital nutrients (23,24). Mitochondrial dysfunction and energy uncoupling are an underlying result of the disruption of oxygen and substrate supply to tissues during ischemia (25).…”

Section: Discussionmentioning

confidence: 99%

Human mesenchymal stromal cells decrease mortality after intestinal ischemia and reperfusion injury

Markel

Crafts

Jensen

et al. 2015

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Human mesenchymal stromal cells decrease mortality after intestinal ischemia and reperfusion injury

Markel

Crafts

Jensen

et al. 2015

Journal of Surgical Research

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“…cells, and vascular endothelial cells (9,18,19,24,54). To confirm that production of soluble mediators was sustained in rhodamine 6G-treated MSCs, angiopoietin 1 and IL-8 levels were quantified after LPS treatment with or without rhodamine 6G pretreatment.…”

Section: Original Articlementioning

confidence: 99%

Mesenchymal Stromal Cells Modulate Macrophages in Clinically Relevant Lung Injury Models by Extracellular Vesicle Mitochondrial Transfer

Morrison

Jackson

Cunningham

et al. 2017

Am J Respir Crit Care Med

541

479

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Rationale: Acute respiratory distress syndrome (ARDS) remains a major cause of respiratory failure in critically ill patients. Mesenchymal stromal cells (MSCs) are a promising candidate for a cell-based therapy. However, the mechanisms of MSCs' effects in ARDS are not well understood. In this study, we focused on the paracrine effect of MSCs on macrophage polarization and the role of extracellular vesicle (EV)-mediated mitochondrial transfer.Objectives: To determine the effects of human MSCs on macrophage function in the ARDS environment and to elucidate the mechanisms of these effects.Methods: Human monocyte-derived macrophages (MDMs) were studied in noncontact coculture with human MSCs when stimulated with LPS or bronchoalveolar lavage fluid (BALF) from patients with ARDS. Murine alveolar macrophages (AMs) were cultured ex vivo with/without human MSC-derived EVs before adoptive transfer to LPS-injured mice.Measurements and Main Results: MSCs suppressed cytokine production, increased M2 macrophage marker expression, and augmented phagocytic capacity of human MDMs stimulated with LPS or ARDS BALF. These effects were partially mediated by CD44-expressing EVs. Adoptive transfer of AMs pretreated with MSCderived EVs reduced inflammation and lung injury in LPS-injured mice. Inhibition of oxidative phosphorylation in MDMs prevented the modulatory effects of MSCs. Generating dysfunctional mitochondria in MSCs using rhodamine 6G pretreatment also abrogated these effects.Conclusions: In the ARDS environment, MSCs promote an antiinflammatory and highly phagocytic macrophage phenotype through EV-mediated mitochondrial transfer. MSC-induced changes in macrophage phenotype critically depend on enhancement of macrophage oxidative phosphorylation. AMs treated with MSCderived EVs ameliorate lung injury in vivo.

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“…TNTs have been found in various types of cells, such as THP1 monocytes [3] , rat astrocytes and neurons [4] , PC12 cells [1,5] , DU 145 prostate cancer cells [6] , HEK293 cells [1,7] , hematopoietic stem cells and progenitor cells [8] , mouse macrophage J774 cells [9] , TRVb-1 cells [10] , human endothelial progenitor cells [11] , T-cells [12] , natural killer cells [13] , human monocyte-derived macrophages [9,14] , and human mesothelioma cells [15,16] . Studies have shown that TNTs can transfer a wide range of substances, such as cellular organelles [5,[17][18][19] , polyglutamine aggregates [20] , H-Ras [21] , MHC class I molecules [22] , Ca 2+ [3,23,24] , and even human immunodeficiency virus and PrP Sc [12,[25][26][27] . Several studies have suggested that TNT-mediated cargo transport is part of the communication between cells [18,27,28] .…”

Section: Introductionmentioning

confidence: 99%

Tunneling nanotubes between rat primary astrocytes and C6 glioma cells alter proliferation potential of glioma cells

Zhang

2015

Neurosci. Bull.

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The tunneling nanotube (TNT) is a newly discovered, long and thin tubular structure between cells. In this study, we established a co-culture system for rat primary astrocytes and C6 glioma cells and found that TNTs formed between them. Most of the TNTs initiated from astrocytes towards C6 glioma cells. The formation of TNTs depended on p53. In addition, hydrogen peroxide increased the number of TNTs in the co-culture system. Established TNTs reduced the proliferation of C6 glioma cells. Our data suggest that TNTs between astrocytes and glioma cells facilitate substance transfer and therefore alter the properties, including the proliferation potential, of glioma cells.

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Mesenchymal stem cells rescue injured endothelial cells in an in vitro ischemia–reperfusion model via tunneling nanotube like structure-mediated mitochondrial transfer

Cited by 292 publications

References 43 publications

Human mesenchymal stromal cells decrease mortality after intestinal ischemia and reperfusion injury

Human mesenchymal stromal cells decrease mortality after intestinal ischemia and reperfusion injury

Mesenchymal Stromal Cells Modulate Macrophages in Clinically Relevant Lung Injury Models by Extracellular Vesicle Mitochondrial Transfer

Tunneling nanotubes between rat primary astrocytes and C6 glioma cells alter proliferation potential of glioma cells

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