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Myocardial regeneration

Adam Vandergriff, Ke Huang, Deliang Shen, Shiqi Hu, Michael Taylor Hensley, Thomas G Caranasos, Li Qian, Ke Cheng
Rationale: Cardiac stem cell-derived exosomes have been demonstrated to promote cardiac regeneration following myocardial infarction in preclinical studies. Recent studies have used intramyocardial injection in order to concentrate exosomes in the infarct. Though effective in a research setting, this method is not clinically appealing due to its invasive nature. We propose the use of a targeting peptide, cardiac homing peptide (CHP), to target intravenously-infused exosomes to the infarcted heart. Methods: Exosomes were conjugated with CHP through a DOPE-NHS linker...
2018: Theranostics
Jiao Li, Shu-Hong Li, Jun Wu, Richard D Weisel, Alina Yao, William L Stanford, Shi-Ming Liu, Ren-Ke Li
Background: To improve the regenerative capacity of aged individuals, we reconstituted bone marrow (BM) of aged mice with young Sca-1 cells, which repopulated cardiac progenitors and prevented cardiac dysfunction after a myocardial infarction (MI). However, the mechanisms involved were incompletely elucidated. This study aimed to investigate whether young, highly regenerative BM Sca-1 cells exert their cardio-protective effects on the aged heart through reactivation of the epithelial-to-mesenchymal transition (EMT) process...
2018: Theranostics
Shang Wang, Manmohan Singh, Thuy Tien Tran, John Leach, Salavat R Aglyamov, Irina V Larina, James F Martin, Kirill V Larin
Myocardial infarction (MI) leads to cardiomyocyte loss, impaired cardiac function, and heart failure. Molecular genetic analyses of myocardium in mouse models of ischemic heart disease have provided great insight into the mechanisms of heart regeneration, which is promising for novel therapies after MI. Although biomechanical factors are considered an important aspect in cardiomyocyte proliferation, there are limited methods for mechanical assessment of the heart in the mouse MI model. This prevents further understanding the role of tissue biomechanics in cardiac regeneration...
February 1, 2018: Biomedical Optics Express
Holger Lörchner, Christian Widera, Yunlong Hou, Albrecht Elsässer, Henning Warnecke, Evangelos Giannitsis, Jean-Sebastien Hulot, Thomas Braun, Kai C Wollert, Jochen Pöling
BACKGROUND: Regenerating islet-derived protein 3 beta (Reg3β) is a cardiomyocyte-derived chemokine for macrophages that is upregulated after myocardial infarction (MI) in mice. Here, we hypothesized that monitoring Reg3β expression might provide specific information on the degree of cardiac inflammation, which is a key determinant in disease progression and prognosis of patients with acute coronary syndrome (ACS). METHODS AND RESULTS: The expression of Reg3β and other inflammatory markers including C-reactive protein (CRP) and myeloperoxidase (MPO) was measured by immunoblotting at serial time points in the hearts and serum of mice with acute MI...
May 1, 2018: International Journal of Cardiology
Ni Zhu, Bing Yi, Zhifu Guo, Guanxin Zhang, Shengdong Huang, Yongwen Qin, Xianxian Zhao, Jianxin Sun
BACKGROUND/AIMS: Pim-1 is a serine/threonine kinase that is highly expressed in the heart, and exerts potent cardiac protective effects through enhancing survival, proliferation, and regeneration of cardiomyocytes. Its myocardial specific substrates, however, remain unknown. In the present study, we aim to investigate whether Pim-1 modulates myofilament activity through phosphorylation of cardiac troponin I (cTnI), a key component in regulating myofilament function in the heart. METHODS: Coimmunoprecipitation and immunofluorescent assays were employed to investigate the interaction of Pim-1 with cTnI in cardiomyocytes...
March 10, 2018: Cellular Physiology and Biochemistry
Nevin Witman, Makoto Sahara
Major cardiovascular events including myocardial infarction (MI) continue to dominate morbidity rates in the developed world. Although multiple device therapies and various pharmacological agents have been shown to improve patient care and reduce mortality rates, clinicians and researchers alike still lack a true panacea to regenerate damaged cardiac tissue. Over the previous two to three decades, cardiovascular stem cell therapies have held great promise. Several stem cell-based approaches have now been shown to improve ventricular function and are documented in preclinical animal models as well as phase I and phase II clinical trials...
2018: Stem Cells International
Julia Dahlmann, George Awad, Carsten Dolny, Sönke Weinert, Karin Richter, Klaus-Dieter Fischer, Thomas Munsch, Volkmar Leßmann, Marianne Volleth, Martin Zenker, Yaoyao Chen, Claudia Merkl, Angelika Schnieke, Hassina Baraki, Ingo Kutschka, George Kensah
The possibility to generate cardiomyocytes from pluripotent stem cells in vitro has enormous significance for basic research, disease modeling, drug development and heart repair. The concept of heart muscle reconstruction has been studied and optimized in the rat model using rat primary cardiovascular cells or xenogeneic pluripotent stem cell derived-cardiomyocytes for years. However, the lack of rat pluripotent stem cells (rPSCs) and their cardiovascular derivatives prevented the establishment of an authentic clinically relevant syngeneic or allogeneic rat heart regeneration model...
2018: PloS One
Hannah J Whittington, Philip J Ostrowski, Debra J McAndrew, Fang Cao, Andrew Shaw, Thomas R Eykyn, Hannah Lake, Jack Tyler, Jurgen E Schneider, Stefan Neubauer, Sevasti Zervou, Craig A Lygate
Aims: Mitochondrial creatine kinase (MtCK) couples ATP production via oxidative phosphorylation to phosphocreatine in the cytosol, which acts as a mobile energy store available for regeneration of ATP at times of high demand. We hypothesised that elevating MtCK would be beneficial in ischaemia-reperfusion (I/R) injury. Methods and Results: Mice were created overexpressing the sarcomeric MtCK gene with αMHC promoter at the Rosa26 locus (MtCK-OE) and compared with wild-type (WT) littermates...
March 2, 2018: Cardiovascular Research
E L Lushnikova, D E Semenov, D B Nikityuk, E V Koldysheva, M G Klinnikova
The study examined the myocardial ultrastructural alterations in rats maintained on various atherogenic diets. It revealed the complex ultrastructural alterations of cardiomyocytes and endotheliocytes (including the lytic and destructive changes of the intracellular organelles, upregulation of the autophagocytosis in the cardiomyocytes, and necrobiosis with apoptosis of endotheliocytes) reflecting the cytopathic features of circulating cholesterol and lipoproteins, whose elevation determined the intensity of destructive processes...
March 5, 2018: Bulletin of Experimental Biology and Medicine
Tamer M A Mohamed, Yen-Sin Ang, Ethan Radzinsky, Ping Zhou, Yu Huang, Arye Elfenbein, Amy Foley, Sergey Magnitsky, Deepak Srivastava
Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a combination of cell-cycle regulators that induce stable cytokinesis in adult post-mitotic cells. We screened cell-cycle regulators expressed in proliferating fetal cardiomyocytes and found that overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 efficiently induced cell division in post-mitotic mouse, rat, and human cardiomyocytes...
February 22, 2018: Cell
Ming Hu, Guixian Guo, Qiang Huang, Chuanfang Cheng, Ruqin Xu, Aiqun Li, Ningning Liu, Shiming Liu
Stem cell therapy can be used to repair and regenerate damaged hearts tissue; nevertheless, the low survival rate of transplanted cells limits their therapeutic efficacy. Recently, it has been proposed that exosomes regulate multiple cellular processes by mediating cell survival and communication among cells. The following study investigates whether injured cardiomyocytes-derived exosomes (cardiac exosomes) affect the survival of transplanted bone marrow mesenchymal stem cells (BMSCs) in infarcted heart. To mimic the harsh microenvironment in infarcted heart that the cardiomyocytes or transplanted BMSCs encounter in vivo, cardiomyocytes conditioned medium and cardiac exosomes collected from H2 O2 -treated cardiomyocytes culture medium were cultured with BMSCs under oxidative stress in vitro...
March 2, 2018: Cell Death & Disease
Chao Wang, Hongsen Du, Jiqiu Hou, Shasha Yan, Jingjing Yang, Yun Wang, Xiujing Zhang, Lili Zhu, Haibin Zhao
Ischemic myocardium initiates the mobilization and homing of bone marrow mesenchymal stem cells (BM-MSCs) to promote myocardial regeneration after acute myocardial infarction (AMI). Inflammation caused by necrotic cardiomyocytes induce major pathological changes (cardiac remodeling and myocardial apoptosis) as well as anxiety disorder. This process may be inhibited by the differentiation and paracrine effects of BM-MSCs. However, the spontaneous mobilization of BMSCs is insufficient to prevent this effect. Given the anti-inflammatory effects of BM-MSCs, ventricular remodeling and anxiety following AMI, methods focused on enhancing BMSCs mobilization are promising...
February 27, 2018: Scientific Reports
Juan Manuel González-Rosa, Michka Sharpe, Dorothy Field, Mark H Soonpaa, Loren J Field, Caroline E Burns, C Geoffrey Burns
Correlative evidence suggests that polyploidization of heart muscle, which occurs naturally in post-natal mammals, creates a barrier to heart regeneration. Here, we move beyond a correlation by demonstrating that experimental polyploidization of zebrafish cardiomyocytes is sufficient to suppress their proliferative potential during regeneration. Initially, we determined that zebrafish myocardium becomes susceptible to polyploidization upon transient cytokinesis inhibition mediated by dominant-negative Ect2...
February 26, 2018: Developmental Cell
Andrew B Goldstone, Cassandra E Burnett, Jeffery E Cohen, Michael J Paulsen, Anahita Eskandari, Bryan E Edwards, Arnar B Ingason, Amanda N Steele, Jay B Patel, John W MacArthur, Judith A Shizuru, Y Joseph Woo
Stromal cell-derived factor 1-alpha (SDF) is a potent bone marrow chemokine capable of recruiting circulating progenitor populations to injured tissue. SDF has known angiogenic capabilities, but bone marrow-derived cellular contributions to tissue regeneration remain controversial. Bone marrow from DsRed-transgenic donors was transplanted into recipients to lineage-trace circulating cells after myocardial infarction (MI). SDF was delivered post-MI, and hearts were evaluated for recruitment and plasticity of bone marrow-derived populations...
February 21, 2018: Journal of Cardiovascular Translational Research
Abdalla Ahmed, Tao Wang, Paul Delgado-Olguin
The neonatal mouse heart has the remarkable capacity to regenerate lost myocardium within the first week of life. Neonatal cardiomyocytes re-express fetal genes that control cell proliferation after injury to promote regeneration. The loss of regenerative capacity of the heart one week after birth coincides with repression of a fetal transcriptional program coordinated by epigenetic regulators. The histone methyltransferase enhancer of zeste homolog 2 (Ezh2) is a repressor of fetal cardiac transcriptional programs and suppresses cardiomyocyte cell proliferation, suggesting a potential function in heart regeneration...
2018: PloS One
I S Stafeev, M Y Menshikov, V A Tkachuk, E V Parfenova
A new trend in modern experimental cardiology is the development of approaches to correction of reparation after myocardial infarction (MI) with the use of specific effects on immune cells. One of the main targets for such interventions is the process of macrophage's polarization in the infarction zone. Proinflammatory M1‑macrophages contribute to hampered myocardial repair, in contrast to M2‑macrophages that promote regeneration. Currently, there are two main ways of targeted delivery of agents necessary for macrophage reprogramming - inlipoid and inglycan-encapsulated particles...
December 2017: Kardiologiia
Raiyan T Zaman, Silvan Tuerkcan, Morteza Mahmoudi, Toshinobu Saito, Phillip C Yang, Frederick T Chin, Michael V McConnell, Lei Xing
OBJECTIVES: Myocardial infarction (MI) causes significant loss of cardiomyocytes, myocardial tissue damage, and impairment of myocardial function. The inability of cardiomyocytes to proliferate prevents the heart from self-regeneration. The treatment for advanced heart failure following an MI is heart transplantation despite the limited availability of the organs. Thus, stem-cell-based cardiac therapies could ultimately prevent heart failure by repairing injured myocardium that reverses cardiomyocyte loss...
2018: PloS One
Raphael F P Castellan, Marco Meloni
While a regenerative response is limited in the mammalian adult heart, it has been recently shown that the neonatal mammalian heart possesses a marked but transient capacity for regeneration after cardiac injury, including myocardial infarction. These findings evidence that the mammalian heart still retains a regenerative capacity and highlights the concept that the expression of distinct molecular switches (that activate or inhibit cellular mechanisms regulating tissue development and regeneration) vary during different stages of life, indicating that cardiac regeneration is an age-dependent process...
2018: Frontiers in Cardiovascular Medicine
Wei Huang, Yuliang Feng, Jialiang Liang, Hao Yu, Cheng Wang, Boyu Wang, Mingyang Wang, Lin Jiang, Wei Meng, Wenfeng Cai, Mario Medvedovic, Jenny Chen, Christian Paul, W Sean Davidson, Sakthivel Sadayappan, Peter J Stambrook, Xi-Yong Yu, Yigang Wang
The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 (miR-128) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of miR-128 impairs CM proliferation and cardiac function, while miR-128 deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses p27 (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2...
February 16, 2018: Nature Communications
Esther Aix, Alex Gallinat, Ignacio Flores
Although recent advances have overturned the old view of the human heart as an inert postmitotic organ, it is clear that the adult heart´s capacity to regenerate after an ischemic episode is very limited. Unlike humans, zebrafish and other lower vertebrates vigorously regenerate damaged myocardium after cardiac injury. Understanding how the zebrafish is able to conserve life-long cardiac regeneration capacity while mammals lose it soon after birth is crucial for the development of new treatments for myocardial infarction...
February 3, 2018: Differentiation; Research in Biological Diversity
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