Thrombosis Research

2013

DOI: 10.1016/j.thromres.2013.04.002

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Allogeneic bone marrow mesenchymal stem cells transplantation for stabilizing and repairing of atherosclerotic ruptured plaque

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Function Of Mscs In Atherosclerosis2

Mesenchymal Stem Cells2

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Cited by 20 publications

(30 citation statements)

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“…A promising alternative is to use MSCs. MSCs can recruit and promote the generation of Tregs (75, 88). Indeed, MSC treatment has significantly increased the number and function of Tregs in cultured splenocytes.…”

Section: Function Of Mscs In Atherosclerosismentioning

confidence: 99%

“…The carboxyfluorescein succinimidyl ester-labeled mMSCs are found in areas close to the endothelium at 7 days after the injection while S-MSCs migrate to atherosclerotic plaque and selectively take up residence near macrophages (77, 81). The transplanted BM-MSCs are able to “home in” on the ruptured plaque regions and differentiate into ECs and collagen fibers (75). BrdU-labeled BM-MSCs are observed in ruptured plaques 4 weeks after the MSC transplantation.…”

Section: Function Of Mscs In Atherosclerosismentioning

confidence: 99%

See 1 more Smart Citation

Function and Therapeutic Potential of Mesenchymal Stem Cells in Atherosclerosis

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2017

Front. Cardiovasc. Med.

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Atherosclerosis is a complicated disorder and largely attributable to dyslipidaemia and chronic inflammation. Despite therapeutic advances over past decades, atherosclerosis remains the leading cause of mortality worldwide. Due to their capability of immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have evolved as an attractive therapeutic agent in various diseases including atherosclerosis. Accumulating evidences support the protective role of MSCs in all stages of atherosclerosis. In this review, we highlight the current understanding of MSCs including their characteristics such as molecular markers, tissue distribution, migratory property, immune-modulatory competence, etc. We also summarize MSC functions in animal models of atherosclerosis. MSC transplantation is able to modulate cytokine and chemokine secretion, reduce endothelial dysfunction, promote regulatory T cell function, decrease dyslipidemia, and stabilize vulnerable plaques during atherosclerosis development. In addition, MSCs may migrate to lesions where they develop into functional cells during atherosclerosis formation. Finally, the perspectives of MSCs in clinical atherosclerosis therapy are discussed.

“…A promising alternative is to use MSCs. MSCs can recruit and promote the generation of Tregs (75, 88). Indeed, MSC treatment has significantly increased the number and function of Tregs in cultured splenocytes.…”

Section: Function Of Mscs In Atherosclerosismentioning

confidence: 99%

“…The carboxyfluorescein succinimidyl ester-labeled mMSCs are found in areas close to the endothelium at 7 days after the injection while S-MSCs migrate to atherosclerotic plaque and selectively take up residence near macrophages (77, 81). The transplanted BM-MSCs are able to “home in” on the ruptured plaque regions and differentiate into ECs and collagen fibers (75). BrdU-labeled BM-MSCs are observed in ruptured plaques 4 weeks after the MSC transplantation.…”

Section: Function Of Mscs In Atherosclerosismentioning

confidence: 99%

Function and Therapeutic Potential of Mesenchymal Stem Cells in Atherosclerosis

¹

,

²

,

³

2017

Front. Cardiovasc. Med.

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Atherosclerosis is a complicated disorder and largely attributable to dyslipidaemia and chronic inflammation. Despite therapeutic advances over past decades, atherosclerosis remains the leading cause of mortality worldwide. Due to their capability of immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have evolved as an attractive therapeutic agent in various diseases including atherosclerosis. Accumulating evidences support the protective role of MSCs in all stages of atherosclerosis. In this review, we highlight the current understanding of MSCs including their characteristics such as molecular markers, tissue distribution, migratory property, immune-modulatory competence, etc. We also summarize MSC functions in animal models of atherosclerosis. MSC transplantation is able to modulate cytokine and chemokine secretion, reduce endothelial dysfunction, promote regulatory T cell function, decrease dyslipidemia, and stabilize vulnerable plaques during atherosclerosis development. In addition, MSCs may migrate to lesions where they develop into functional cells during atherosclerosis formation. Finally, the perspectives of MSCs in clinical atherosclerosis therapy are discussed.

“…The vehicle-treated group was injected with an equal volume of PBS alone. All rabbits were administered antibiotics for 3 days after the procedure to prevent infection [23]. …”

Section: Methodsmentioning

confidence: 99%

Autologous Bone Marrow Mononuclear Cell Transplantation Delays Progression of Carotid Atherosclerosis in Rabbits

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et al. 2015

Mol Neurobiol

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Background Bone marrow mononuclear cells (BMMNCs) can counteract oxidative stress and inhibit the inflammatory response in focal ischemic stroke models. However, the effect of BMMNC transplantation on carotid atherosclerosis needs to be determined. Methods The carotid atherosclerotic plaque model was established in New Zealand White rabbits by balloon injury and 8 weeks of high-fat diet. Rabbits were randomized to receive an intravenous injection of autologous BrdU-labeled BMMNCs or an equal volume of phosphate-buffered saline. Plaques were evaluated for expression of proinflammatory and anti-inflammatory cytokines, antioxidant proteins, and markers of cell death. Results BMMNCs migrated into atherosclerotic plaque on the first day after cell transplantation. BMMNC-treated rabbits had smaller plaques and more collagen deposition than did the vehicle-treated controls on day 28 (p<0.05). BMMNC treatment significantly increased endothelial nitric oxide synthase and the antioxidant enzymes glutathione peroxidase and superoxide dismutase in plaques compared to vehicle treatment on day 7. BMMNC-treated rabbits also had lower levels of cleaved caspase-3 expression; lower levels of proinflammatory cytokines interleukin-1β, tumor necrosis factor-α, and matrix metalloproteinase 9; and higher levels of insulin-like growth factor-1 and its receptor (p<0.05). Conclusions Autologous BMMNC transplantation can suppress the process of atherosclerotic plaque formation and is associated with enhanced antioxidative effect, reduced levels of inflammatory cytokines and cleaved caspase-3, and increased expression of insulin-like growth factor-1 and its receptor. BMMNC transplantation represents a novel approach for the treatment of carotid atherosclerosis.

“…To stabilize the plaque, some investigators explored the possibility of cell therapy via infusion of mesenchymal stem cells or smooth muscle progenitors. 52 Allogeneic bone marrow mesenchymal stem cell transplantation showed an important role in the stabilization and repair of ruptured atherosclerotic plaque. 52 Furthermore, matrix metalloproteinase-8 expressed in stem/progenitor cells plays a part in mediating cell migration and their recruitment into atherosclerotic lesions.…”

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

“…52 Allogeneic bone marrow mesenchymal stem cell transplantation showed an important role in the stabilization and repair of ruptured atherosclerotic plaque. 52 Furthermore, matrix metalloproteinase-8 expressed in stem/progenitor cells plays a part in mediating cell migration and their recruitment into atherosclerotic lesions. 53 The number of stem/progenitor cells in atheroma was significantly reduced by genetic deletion of matrix metalloproteinase-8 in apolipoprotein E-deficient mice fed a Western diet.…”

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

Stem/Progenitor Cells in Vascular Regeneration

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2014

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