Concomitant Retrograde Coronary Venous Infusion of Basic Fibroblast Growth Factor Enhances Engraftment and Differentiation of Bone Marrow Mesenchymal Stem Cells for Cardiac Repair after Myocardial Infarction

Xiao, Wang; Lei, Zhen; Miao, Heng; Sun, Qiwei; Yang, Yali; Qu, Bin; Lao, Edmundo Patricio Lopes; Wu, Xing-Xin; Ren, Hongmei; Shi, Shutian; Ma, Xin‐Liang; Ma, Changsheng; Nie, Shaoping

doi:10.7150/thno.11607

Cited by 32 publications

(23 citation statements)

References 37 publications

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“…Having mentioned this, the combined effect of BM-MSCs along with basic fibroblast growth factor ( bFGF )-binding ECM has been observed to improve the left ventricular (LV) function and enhance myocardial regeneration [ 69 ]. One of the most effective delivery methods for the treatment has been observed to be via the retrograde infusion of the two [ 70 ]. Mixed treatment of BM-MSCs with endothelial progenitor cells (EPCs) pre-treated with salvianolic acid B results in reduced infarct area and enhanced stem cell proliferation [ 71 ].…”

Section: Main Textmentioning

confidence: 99%

Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010–2015)

2016

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Mesenchymal stem cells have been used for cardiovascular regenerative therapy for decades. These cells have been established as one of the potential therapeutic agents, following several tests in animal models and clinical trials. In the process, various sources of mesenchymal stem cells have been identified which help in cardiac regeneration by either revitalizing the cardiac stem cells or revascularizing the arteries and veins of the heart. Although mesenchymal cell therapy has achieved considerable admiration, some challenges still remain that need to be overcome in order to establish it as a successful technique. This in-depth review is an attempt to summarize the major sources of mesenchymal stem cells involved in myocardial regeneration, the significant mechanisms involved in the process with a focus on studies (human and animal) conducted in the last 6 years and the challenges that remain to be addressed.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-016-0341-0) contains supplementary material, which is available to authorized users.

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Section: Main Textmentioning

confidence: 99%

Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010–2015)

2016

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“…Because of their many advantages, such as ease of isolation and culture, their directional migration and lack of immune rejection, MSCs are considered to have great therapeutic potential for many diseases . Injection of MSCs has been utilized to alleviate atherosclerosis, myocardial ischaemia and vascular balloon injury . Experiments have shown that oxidative stress exists in vascular intima and the blood circulation following both vein grafting and vascular injury, after a short period of time and lasting for several weeks .…”

Section: Introductionmentioning

confidence: 99%

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

Bai

et al. 2017

J Cellular Molecular Medi

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The oxidative stress caused by endothelial injury is involved in intimal hyperplasia (IH) in vein grafts. Mesenchymal stem cells (MSCs) can home to injured intima and promote endothelial repair. However, MSC apoptosis is increased accompanied by decreased functional activity under oxidative stress. Thus, we investigate whether tumour necrosis factor‐α (TNF‐α) can promote the survival and activity of MSCs under oxidative stress to reduce IH more effectively, and establish what role the NF‐κB pathway plays in this. In this study, we preconditioned MSCs with TNF‐α (TNF ‐α‐PCMSCs) for 24 hrs and measured the activation of the IKK/NF‐κB pathway. EdU and transwell assays were performed to assess proliferation and migration of TNF ‐α‐PCMSCs. Apoptosis and migration of TNF ‐α‐ PCMSCs were evaluated in conditions of oxidative stress by analysis of the expression of Bcl‐2 and CXCR4 proteins. TNF ‐α‐ PCMSCs were transplanted into a vein graft model, so that cell homing could be tracked, and endothelial apoptosis and IH of vein grafts were measured. The results demonstrated that TNF‐α promotes proliferation and migration of MSCs. Furthermore, survival and migration of TNF ‐α‐ PCMSCs under oxidative stress were both enhanced. A greater number of MSCs migrated to the intima of vein grafts after preconditioning with TNF‐α, and the formation of neointima was significantly reduced. These effects could be partially abolished by IKK XII (NF‐κB inhibitor). All these results indicate that preconditioning with TNF‐α can promote survival and migration of MSCs under oxidative stress via the NF‐κB pathway and thus attenuate IH of vein grafts.

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“…TGF-β1 may stimulate the proliferation of mesenchymal stem cells and induce their differentiation into osteoblasts 33, 34; the low concentration of TGF-β1 promotes the maturation of osteoclasts 35. These process couple bone resorption with bone formation 26, 36, 37.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of ATP6V1H Causes Bone Loss by Inhibiting Bone Resorption and Bone Formation through the TGF-β1 Pathway

et al. 2016

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Vacuolar-type H +-ATPase (V-ATPase) is a highly conserved, ancient enzyme that couples the energy of ATP hydrolysis to proton transport across vesicular and plasma membranes of eukaryotic cells. Previously reported mutations of various V-ATPase subunits are associated with increased bone density. We now show that haploinsufficiency for the H subunit of the V1 domain (ATP6V1H) is associated with osteoporosis in humans and mice. A genome-wide SNP array analysis of 1625 Han Chinese found that 4 of 15 tag SNPs (26.7%) within ATP6V1H were significantly associated with low spine bone mineral density. Atp6v1h+/- knockout mice generated by the CRISPR/Cas9 technique had decreased bone remodeling and a net bone matrix loss. Atp6v1h+/- osteoclasts showed impaired bone formation and increased bone resorption. The increased intracellular pH of Atp6v1h+/- osteoclasts downregulated TGF-β1 activation, thereby reducing induction of osteoblast formation but the bone mineralization was not altered. However, bone formation was reduced more than bone resorption. Our data provide evidence that partial loss of ATP6V1H function results in osteoporosis/osteopenia. We propose that defective osteoclast formation triggers impaired bone formation by altering bone remodeling. In the future, ATP6V1H might, therefore, serve as a target for the therapy of osteoporosis.

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Concomitant Retrograde Coronary Venous Infusion of Basic Fibroblast Growth Factor Enhances Engraftment and Differentiation of Bone Marrow Mesenchymal Stem Cells for Cardiac Repair after Myocardial Infarction

Cited by 32 publications

References 37 publications

Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010–2015)

Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010–2015)

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

Deficiency of ATP6V1H Causes Bone Loss by Inhibiting Bone Resorption and Bone Formation through the TGF-β1 Pathway

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