How to Improve the Survival of Transplanted Mesenchymal Stem Cell in Ischemic Heart?

Li, Liangpeng; Chen, Xiongwen; Wang, Wei Eric; Zeng, Chunyu

doi:10.1155/2016/9682757

Cited by 190 publications

(188 citation statements)

References 139 publications

(141 reference statements)

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“…Although the high rates of iPSC apoptosis are a painful reminder of the fundamental challenges associated with cellular engraftment techniques, the paracrine effect of iPSCs should not go unexamined. 86 Indeed the authors of this study provided evidence of neotissue formation brought about by the presence of iPSCs.…”

Section: Tissue-engineered Blood Vesselsmentioning

confidence: 69%

“…73 Techniques seeking to improve their adhesion and integration into host tissue are vital if iPSC-derived tissue engineering is to be pursued. Reports of transplanted stem cells releasing soluble factors, resulting in a paracrine effect on neighboring cells, 85,86,101 would suggest that iPSC-derived VSMCs contribute to cardiovascular repair and regeneration may occur through a similar manner as seen with the study by Hibino et al 102 using iPSC sheets.…”

Section: Challenges In Ipsc-derived Vsmcsmentioning

confidence: 88%

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Differentiation and Application of Induced Pluripotent Stem Cell–Derived Vascular Smooth Muscle Cells

Maguire

Xiao

2017

ATVB

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Abstract-Vascular smooth muscle cells (VSMCs) play a role in the development of vascular disease, for example, neointimal formation, arterial aneurysm, and Marfan syndrome caused by genetic mutations in VSMCs, but little is known about the mechanisms of the disease process. Advances in induced pluripotent stem cell technology have now made it possible to derive VSMCs from several different somatic cells using a selection of protocols. As such, researchers have set out to delineate key signaling processes involved in triggering VSMC gene expression to grasp the extent of gene regulatory networks involved in phenotype commitment. This technology has also paved the way for investigations into diseases affecting VSMC behavior and function, which may be treatable once an identifiable culprit molecule or gene has been repaired. Moreover, induced pluripotent stem cell-derived VSMCs are also being considered for their use in tissue-engineered blood vessels as they may prove more beneficial than using autologous vessels. Finally, while several issues remains to be clarified before induced pluripotent stem cell-derived VSMCs can become used in regenerative medicine, they do offer both clinicians and researchers hope for both treating and understanding vascular disease. In this review, we aim to update the recent progress on VSMC generation from stem cells and the underlying molecular mechanisms of VSMC differentiation. We will also explore how the use of induced pluripotent stem cell-derived VSMCs has changed the game for regenerative medicine by offering new therapeutic avenues to clinicians, as well as providing researchers with a new platform for modeling of vascular disease. Visual Overview-An online visual overview is available for this article.

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Section: Tissue-engineered Blood Vesselsmentioning

confidence: 69%

Section: Challenges In Ipsc-derived Vsmcsmentioning

confidence: 88%

Differentiation and Application of Induced Pluripotent Stem Cell–Derived Vascular Smooth Muscle Cells

Maguire

Xiao

2017

ATVB

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“…Various strategies have been tested to overcome the low survival rate of stem cells after transplantation in heart tissue, but due to different measurements were used in these studies, a unified standard that measuring the efficacies of approaches improving cell retention is required to determine the optimal strategy [57] . In addition, human embryonic stem cell (hESC) and inducible functional stem cell (iPSC) lines showed increased frequency of specific gene aberrations, thus, it requires frequent genetic testing of pluripotent stem cells to ensure its stability and clinical safety [58,59] .…”

Section: Resultsmentioning

confidence: 99%

New Strategies for Myocardial Infarction Treatment

Peng

Zhou

2017

Journal of Cardiology and Therapy

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At present, the treatments of myocardial infarction mainly focus on the recanalization of the occluded coronary artery to restore perfusion and prevent myocardial necrosis. To do this, commonly used methods include drug therapy, thrombolytic therapy, percutaneous coronary intervention (PCI), and coronary artery bypass graft (CABG) surgery. Drug therapiesTraditional drug therapies include angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs), aldosterone receptor antagonists, β-receptor blockers, and so on [1][2][3] . The main purpose of these treatments is the prevention of left ventricular remodeling. Thrombolytic therapy ABSTRACTMyocardial infarction is due to lasting and serious myocardial ischemia that leads to myocardial necrosis and cardiac remodeling, and can consequently result in heart failure. Traditional treatment for myocardial infarction includes drug therapy, thrombolytic therapy, percutaneous coronary intervention (PCI), and coronary artery bypass graft (CABG) surgery. Although these treatments can to some extent relieve the symptom of myocardial ischemia, they fail to repair the necrotic heart tissues. Myocardial regeneration is undoubtedly the best solution to the clinical problems of myocardial infarction treatment. The review briefly illustrated the pros and cons of the traditional treatments of myocardial infarction, and focused on the application of new strategies for myocardial infarction treatment using myocardial regeneration.

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“…at ischemic area jeopardies engraftment and execution of the repair mechanisms the transplanted stem cells and eventually causes cell death. 16,19,20 This emphasizes the importance of conducive micro-environment in delivering the expected therapeutical effects of stem cells. However, it is also equivalently crucial to elucidate the response and homeostasis behavior of stem cells when transplanted or homed at non-conducive microenvironments.…”

Section: Discussionmentioning

confidence: 99%

Impaired redox environment modulates cardiogenic and ion-channel gene expression in cardiac-resident and non-resident mesenchymal stem cells

Baskar¹,

Subbannagounder²,

Ramanathanpullai³

et al. 2017

Exp Biol Med (Maywood)

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Human mesenchymal stem cells (h-MSCs) are highly promising candidates for tissue repair in cardiovascular diseases. However, the retention of cells in the infarcted area has been a major challenge due to its poor viability and/or low survival rate after transplantation. The regenerative potential of mesenchymal stem cells (MSCs) repudiate and enter into premature senescence via oxidative stress. Thus, various strategies have been attempted to improve the MSC survival in 'toxic' conditions. Similarly, we investigated the response of cardiac resident MSC (hCMSCs) and non-resident MSCs against the oxidative stress induced by H 2 O 2 . Supplementation of ascorbic acid (AA) into MSCs culture profoundly rescued the stem cells from oxidative stress induced by H 2 O 2 . Our data showed that the pretreatment of AA is able to inhibit the cell death and thus preserving the viability and differentiation potential of MSCs. AbstractRedox homeostasis plays a crucial role in the regulation of self-renewal and differentiation of stem cells. However, the behavioral actions of mesenchymal stem cells in redox imbalance state remain elusive. In the present study, the effect of redox imbalance that was induced by either hydrogen peroxide (H 2 O 2 ) or ascorbic acid on human cardiac-resident (hC-MSCs) and non-resident (umbilical cord) mesenchymal stem cells (hUC-MSCs) was evaluated. Both cells were sensitive and responsive when exposed to either H 2 O 2 or ascorbic acid at a concentration of 400 mmol/L. Ascorbic acid pre-treated cells remarkably ameliorated the reactive oxygen species level when treated with H 2 O 2 . The endogenous antioxidative enzyme gene (Sod1, Sod2, TRXR1 and Gpx1) expressions were escalated in both MSCs in response to reactive oxygen species elevation. In contrast, ascorbic acid pre-treated hUCMSCs attenuated considerable anti-oxidative gene (TRXR1 and Gpx1) expressions, but not the hC-MSCs. Similarly, the cardiogenic gene (Nkx 2.5, Gata4, Mlc2a and b-MHC) and ionchannel gene (I KDR , I KCa , I to and I Na.TTX ) expressions were significantly increased in both MSCs on the oxidative state. On the contrary, reduced environment could not alter the ionchannel gene expression and negatively regulated the cardiogenic gene expressions except for troponin-1 in both cells. In conclusion, redox imbalance potently alters the cardiacresident and non-resident MSCs stemness, cardiogenic, and ion-channel gene expressions. In comparison with cardiac-resident MSC, non-resident umbilical cord-MSC has great potential to tolerate the redox imbalance and positively respond to cardiac regeneration.

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How to Improve the Survival of Transplanted Mesenchymal Stem Cell in Ischemic Heart?

Cited by 190 publications

References 139 publications

Differentiation and Application of Induced Pluripotent Stem Cell–Derived Vascular Smooth Muscle Cells

Differentiation and Application of Induced Pluripotent Stem Cell–Derived Vascular Smooth Muscle Cells

New Strategies for Myocardial Infarction Treatment

Impaired redox environment modulates cardiogenic and ion-channel gene expression in cardiac-resident and non-resident mesenchymal stem cells

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