Transplantation of Isl1+ cardiac progenitor cells in small intestinal submucosa improves infarcted heart function

Wang, Lingjun; Meier, Elizabeth M.; Tian, Shuo; Lei, Ienglam; Liu, Liu; Xian, Shaoxiang; Lam, Mai T.; Wang, Zhong

doi:10.1186/s13287-017-0675-2

Cited by 32 publications

(18 citation statements)

References 46 publications

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“…A pilot study of cell-based therapies was introduced by Asahara et al, who observed that EPCs, isolated from human peripheral blood, contributed to vessel growth in ischemic tissues. This angiogenic potential has been replicated in clinical studies using cardiac progenitor cells [31,32] and ASCs [33]. However, excitement about EPCs and their phenotype, origin, and mechanism has been dampened because of unresolved questions, despite results demonstrating improved neovascularization in animal models of ischemia [34].…”

Section: Stem/progenitor Cell Therapymentioning

confidence: 99%

Approaches to therapeutic angiogenesis for ischemic heart disease

et al. 2018

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Ischemic heart disease (IHD) is caused by the narrowing of arteries that work to provide blood, nutrients, and oxygen to the myocardial tissue. The worldwide epidemic of IHD urgently requires innovative treatments despite the significant advances in medical, interventional and surgical therapies for this disease. Angiogenesis is a physiological and pathophysiological process that initiates vascular growth from pre-existing blood vessels in response to a lack of oxygen. This process occurs naturally over time and has encouraged researchers and clinicians to investigate the outcomes of accelerating or enhancing this angiogenic response as an alternative IHD therapy. Therapeutic angiogenesis has been shown to revascularize ischemic heart tissue, reduce the progression of tissue infarction and evade the need for invasive surgical procedures or tissue/organ transplants. Several approaches, including the use of proteins, genes, stem/progenitor cells and various combinations, have been employed to promote angiogenesis. While clinical trials for these approaches are ongoing, microvesicles and exosomes have recently been investigated as a cell-free approach to stimulate angiogenesis and may circumvent limitations of using viable cells. This review summarizes the approaches to accomplish therapeutic angiogenesis for IHD by

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Section: Stem/progenitor Cell Therapymentioning

confidence: 99%

Approaches to therapeutic angiogenesis for ischemic heart disease

et al. 2018

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“…For example, the SIS is made into a tubule with crosslinking of various biologically active factors and transplanted into animal to substitute carotid arteries [ 23 , 47 ]. SIS was loaded with cardiomyocytes and then was transplanted to the outer surface of infarcted myocardium in mice to repair heart function [ 16 ]. For meniscus reconstruction, meniscus cells and synovial-derived stem cells were also transplanted on SIS [ 19 ].…”

Section: Overview Of Sismentioning

confidence: 99%

Surface modification of small intestine submucosa in tissue engineering

Pan

Qin

et al. 2020

Regenerative Biomaterials

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With the development of tissue engineering, the required biomaterials need to have the ability to promote cell adhesion and proliferation in vitro and in vivo. Especially, surface modification of the scaffold material has a great influence on biocompatibility and functionality of materials. The small intestine submucosa (SIS) is an extracellular matrix isolated from the submucosal layer of porcine jejunum, which has good tissue mechanical properties and regenerative activity, and is suitable for cell adhesion, proliferation and differentiation. In recent years, SIS is widely used in different areas of tissue reconstruction, such as blood vessels, bone, cartilage, bladder and ureter, etc. This paper discusses the main methods for surface modification of SIS to improve and optimize the performance of SIS bioscaffolds, including functional group bonding, protein adsorption, mineral coating, topography and formatting modification and drug combination. In addition, the reasonable combination of these methods also offers great improvement on SIS surface modification. This article makes a shallow review of the surface modification of SIS and its application in tissue engineering.

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“…Recent research documented that CSCs was involved in the heart failure (HF). 3,4 Thus, there need more investigations to investigate the mechanism of the function of CSCs in HF. The hypoxia was reported that involved in the HF.…”

mentioning

confidence: 99%

MALAT1 promoted cell proliferation and migration via MALAT1/miR‐155/MEF2A pathway in hypoxia of cardiac stem cells

Wang

Chen

2018

J of Cellular Biochemistry

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Accumulating evidence revealed that hypoxia contributed to many human diseases, including ischemic myocardium and heart failure (HF). In recent years, the roles of hypoxia in stem cell survival and cardiac biology have been studied extensively. However, the underlying molecular mechanisms remain to be elucidated. As a leading cause of HF, ischemic heart disease was correlated with hypoxia. In this study, we firstly constructed the hypoxia cell model by CoCl2 in cardiac stem cells (CSCs) and found that hypoxia induced the cell proliferation and migration potential in CSCs. Then, we demonstrated that the expression of metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) was promoted in CoCl2‐induced CSCs hypoxia model. Furthermore, we found that knockdown of MALAT1 inhibited the cell proliferation and migration in CoCl2‐induced CSCs hypoxia model. In addition, we revealed that MALAT1 regulated the microRNA‐155 (miR‐155) expression in CSCs under both the normal and hypoxia conditions and further, manipulation of the miR‐155 expression affected the role of MALAT1 in CoCl2‐induced CSCs hypoxia cell model. We then illustrated that miR‐155 regulated the myocyte enhancer factor 2A (MEF2A) expression in CSCs under both the normal and hypoxia conditions and further, changing the expression of MEF2A affected the role of miR‐155. Finally, we demonstrated that MALAT1 regulated the MEF2A expression and exerted its role via modulation of the MALAT1/miR‐155/MEF2A pathway. Taken together, our study illustrated that MALAT1 promoted the cell proliferation and migration in CoCl2‐induced CSCs hypoxia model, acting mechanistically by promoting MEF2A expression via “sponging” miR‐155.

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Transplantation of Isl1+ cardiac progenitor cells in small intestinal submucosa improves infarcted heart function

Cited by 32 publications

References 46 publications

Approaches to therapeutic angiogenesis for ischemic heart disease

Approaches to therapeutic angiogenesis for ischemic heart disease

Surface modification of small intestine submucosa in tissue engineering

MALAT1 promoted cell proliferation and migration via MALAT1/miR‐155/MEF2A pathway in hypoxia of cardiac stem cells

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