Chongfan Technology
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2024
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Construction of human amniotic epithelial stem cell patch epicardial transplantation based on antioxidant polyurethane scaffold for myocardial infarction by Yu Luyang and other teams of Zhejiang University
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Myocardial infarction (MI) is the leading cause of death worldwide. Stem cell therapy is considered a potential strategy for the treatment of myocardial infarction. Classical stem cell transplantation, such as embryonic stem cells, induced pluripotent stem cells and cardiac stem cells, has a certain repair effect on myocardial infarction by supplementing cardiomyocytes. However, due to cell survival, differentiation, functional activity and biological safety and ethical issues, its clinical application is hindered.
On October 22, 2024, Yu Luyang, Gao Changyou and Zhu Yang of Zhejiang University jointly communicatedNature CommunicationsOnline is titled“Epicardial transplantation of antioxidant polyurethane scaffold based human amniotic epithelial stem cell patch for myocardial infarction treatment”The research paper,The studyPorous antioxidant polyurethane (PUR) stem cell cardiac patch was constructed using human amniotic epithelial stem cells (hAESCs) with immunomodulatory activity, immune privilege and biological safety as materials. The patch has good compatibility with hAESCs.
In rats, the PUR-hAESC patch can significantly reduce myocardial fibrosis after myocardial infarction, promote myocardial vascularization, and improve cardiac remodeling and function. Mechanically, the patch provides a beneficial microenvironment for cardiac repair by promoting a desirable immune response, paracrine regulation, and a limited oxidative environment.The findings may provide a potential therapeutic strategy for myocardial infarction.
Myocardial infarction (MI), caused by ischemia following occlusion of a coronary artery, is the leading cause of death, affecting more than 700 million people worldwide each year.In the infarcted heart, extensive cardiomyocyte (CM) death and vascular injury result in the release of pro-inflammatory mediators, including reactive oxygen species (ROS) and pro-inflammatory cytokines. A strong inflammatory response in the infarcted area and nearby tissues can delay repair, aggravate myocardial damage, and lead to fibrosis, which is related to poor tissue remodeling after myocardial infarction and consequent heart failure. However, studies have shown that broadly suppressing inflammation during cardiac repair does not improve cardiac wound healing. Glucocorticoids and NSAIDs are associated with recurrent myocardial infarction and higher mortality in patients with myocardial infarction.To date, there is no approved treatment to reduce infarct size due to irreversible death in patients with myocardial infarction.
In recent years, stem cell-based therapies have attracted attention as a promising strategy for post-infarction cardiac repair.To replenish CM, several types of stem cells, represented by embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), and cardiac stem cells (CSCs), have been introduced into the infarcted heart to help reduce ischemic damage in preclinical and clinical trials. Although this strategy has achieved certain results, the transplanted cells show different degrees of differentiation, low integration rate and survival rate, and abnormal electrophysiological and mechanical functions of the repair heart, which may increase the risk of arrhythmia. All these problems, combined with tumorigenesis, immune rejection, gene mutation and ethical issues, limit clinical applications. Recently, experimental and clinical evidence has demonstrated that the primary role of adult stem cells in the process of cardiac repair is to modulate the immune system, in particular to maintain moderate acute inflammatory activation to promote wound healing, rather than to directly replace dysfunctional myocardium.Therefore, the development of stem cell therapy suitable for regulating the pathological microenvironment of myocardial infarction will provide a more effective intervention strategy for the treatment of myocardial infarction.
Human amniotic epithelial stem cells (hAESCs), a human placental stem cell derived from fetal membranes, are a promising candidate based on their properties demonstrated in other studies and our previous studies.Similar to mesenchymal stem cells (MSCs), hAESCs have the advantages of powerful paracrine and immune regulation. Many placental cell types, including hAESCs, exhibit immune privilege due to a lack of human leukocyte antigen (HLA) class II molecules and high expression of non-classical HLA class I molecules. As placenta-derived cells, hAESCs have many additional advantages, such as ample supply, no ethical concerns, and no additional invasive surgery. As newborn cells, hAESCs have no age-or environment-related DNA damage compared to human adult stem cells. Most importantly, hAESCs are safe stem cells that are genetically stable and do not form tumors when transplanted into volunteers and patients. Compared with iPSCs and ESCs, the non-tumorigenicity and lack of ethical issues of hAESCs are also two major advantages. More importantly, many studies have shown that hAESCs have multiple immunomodulatory activities. hAESCs can secrete beneficial paracrine factors with anti-fibrotic, pro-angiogenic and immunomodulatory properties, such as matrix metalloproteinases (MMP-2, MMP-9), vascular endothelial growth factor (VEGF), angiopoietin (AGN), macrophage migration inhibitory factor (MIF) and indoleamine 2,3-dioxygenase (IDO), which can alter the surrounding cells and microenvironment. In particular, a systematic safety assessment of hAESC was carried out, and based on previous studies, a current good manufacturing practice (cGMP) grade hAESC cell therapy product was developed in a serum-free system.Taken together, these properties make hAESCs attractive for cell therapy of myocardial infarction.
A major obstacle to the effectiveness of cell delivery in cell therapy is the extremely low rate of cell retention and survival in the local pathological microenvironment.Recently, biomaterials have been applied to the treatment of myocardial infarction, promising to address these limitations of cell transplantation. ROS-reactive polyurethane heart patches have been studied for many years, demonstrating that the patch is flexible, elastic, and compatible with cell viability. In addition, ROS-responsive polymers can "intelligently" consume excess ROS and are considered ideal carriers for transplanted cells. A porous antioxidant polyurethane (PUR) scaffold was developed as a carrier for hAESCs to construct a PUR-hAESC heart patch. To improve cell retention, the former antioxidant polyurethane (PFTU) was modified with arginine glycine aspartic acid adhesion peptide (RGD), which is present in fibronectin and plays a role in cell attachment and spreading.In this strategy, the PUR-hAESC patch provides a unique advantage for the survival of hAESCs and significantly improves myocardial infarction by modulating the microenvironment of myocardial infarction.
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