Abstract 548: Cellular Contributions to Neonatal Cardiac Regeneration

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Adwiteeya Misra ◽  
Pearl J Quijada ◽  
Ryan Burke ◽  
Ronald Dirkx ◽  
Eric M Small
Keyword(s):  
Rna Sequencing ◽  
Troponin T ◽  
Cardiac Injury ◽  
Cardiac Regeneration ◽  
Cardiac Repair ◽  
Mouse Heart ◽  
Sequencing Data ◽  
Injury Response ◽  
Virus Serotype

While the neonatal mouse heart possesses a remarkable ability to regenerate up to a week after birth, the adult mammalian heart is susceptible to irreversible scar formation that impedes cardiac function. Such a scar is formed by the precocious deposition of extracellular matrix (ECM) by resident cardiac fibroblasts (CFs). Unlike their adult counterparts, neonatal CFs in the regenerative widow may have a unique phenotype that contributes to cardiac regeneration and scar resolution. Indeed, the neonatal cardiac ECM secreted by CFs is reported to stimulate regeneration, yet the underlying mechanisms of CF-mediated cardiac repair in the neonate has not been examined. Here, we present a strategy to establish the role of tissue resident CFs in mouse neonatal cardiac regeneration through selective cell depletion and RNA sequencing. Through the initial analysis of published RNA sequencing data, we identified an enrichment of pro-regenerative molecules such as amphiregulin (Areg) during the neonatal regenerative window. Areg, an epidermal growth factor ligand, has been shown to paradoxically stimulate both cardiac repair and pathological fibrosis after adult cardiac injury. To assess its impact on the neonatal cardiac injury response, we developed an adeno-associated virus serotype 9 with the complete coding sequence of mouse Areg (AAV9:Areg) controlled by the cardiomyocyte-specific cardiac troponin T promoter. In vivo , AAV9:Areg treated mice accumulate BrdU+ (proliferative) non-myocytes adjacent to Areg-expressing cardiomyocytes. Ongoing studies are aimed at evaluating the contribution of CFs to neonatal cardiac repair, including whether Areg-dependent cellular changes impact CFs in the neonatal regenerative window in a manner distinct from that in the adult injury response.

Abstract 34: Acetylation of GATA 4 Enhanced Direct Cardiac Reprogramming of Induced Cardiomyocytes

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Vivek P Singh ◽  
Megumi Mathison ◽  
Jaya P Pinnamaneni ◽  
Deepthi Sanagasetti ◽  
Narasimhaswamy S Belaguli ◽  
...  
Keyword(s):  
Ventricular Function ◽  
Troponin T ◽  
Novel Mutation ◽  
Cardiac Regeneration ◽  
Negative Control ◽  
Direct Reprogramming ◽  
Wild Type ◽  
Reprogramming Efficiency

Objective: Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) by forced expression of cardiomyogenic factors, GMT (GATA4, Mef2c and Tbx5), has recently been demonstrated, suggesting a promising statregy for cardiac regeneration. However, the efficiency of direct reprogramming is usually relatively low and requires extensive epigenetic redesigning, although the underlying mechanism are largely unknown. Methods: In a recent study, we created a novel mutation in rat GATA 4 by replacing lysine residue with glutamine at position 299 i.e. (K299Q), to mimic constitutive acetylation and examined whether constitutive acetylation of GATA4, when compared with wild type GATA4, further enhance GMT-mediated direct reprogramming efficiency of induced cardiomyocytes in vitro and accordingly ventricular function after myocardial infarction in rat, in vivo . Results: We found that acetylated GATA 4 (K299Q), in the presence of Mef2c and Tbx5 upregulated cardiac-specific markers, suppressed fibroblast genes, in rat cardiac fibroblasts (RCFs) more efficiently when compared with Mef2c, Tbx5 plus wild type GATA4. FACS analyses revealed that G(K299Q) MT induced significantly more cardiomyocyte marker cardiac troponin T (cTnT) expression compared with GMT alone. Mechanistic studies demonstrated that the K299Q substitution, resulting in enriched p300 occupancy at the GATA 4 promoter, induced acetylation of Histine 3, decreased HDAC expression. In addition, substitution augmented the increase in an acetylated form of GATA-4 and its DNA binding and transcriptional activity, compared with wildtype GATA 4. In agreement with upregulated cTNT gene expression in vitro , echocardiographic analysis demonstrate that the acetylated G(K299Q) MT vectors have improved effect in enhancing ventricular function than GMT vectors from postinfarct baselines as compared to negative control [G(K299Q) MT, 15.6% ± 2.7%; G(WT)MT, 12.8% ± 1.7%; GFP, -2.3% ± 1.1%]. Conclusions: Collectivily, these data indicate that acetylated GATA4 (K299Q) significantly increases reprogramming efficiency of induced cardiomyocytes (iCMs), in vitro and in vivo, and provide new insight into the molecular mechanism underlying cardiac regeneration.

Abstract 15: Limiting GRK2 in the Ischemic Heart can Promote Cardiac Regeneration

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Maria Cecilia Scimia ◽  
Lin Zuo ◽  
Kate E Sydnes ◽  
Daniel A Zuppo ◽  
Erhe Gao ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Cardiac Injury ◽  
Cardiac Regeneration ◽  
Cardiac Repair ◽  
Functional Improvement ◽  
Coronary Artery Ligation ◽  
Therapeutic Effects ◽  
Artery Ligation ◽  
C Terminus ◽  
Independent Effects

The detrimental role of G protein-coupled receptor (GPCR) kinase (GRK2) following cardiac injury/stress has been documented over the last two decades. Importantly, our lab has shown that inhibition or deletion of GRK2 in cardiomyocytes can prevent and also rescue heart failure (HF) phenotypes. Its role in GPCR desensitization including regulation of β-adrenergic receptors (βARs) during HF development has been well characterized. However, recently our lab and others have found that GRK2 can have novel GPCR-independent effects in the heart that appear to contribute to its pathological effects and thus, inhibition of these actions of GRK2 may contribute to therapeutic effects seen. In this study we explored whether the cardiac repair observed with lower myocardial GRK2 might involve regenerative processes. In cardiac-specific GRK2 knockout (KO) mice and also transgenic mice with cardiac-targeted expression of the βARKct, a peptide inhibitor of GRK2 activation via Gβγ sequestration, we induced HF via coronary artery ligation and subsequent myocardial infarction (MI) and measured aspects of cardiac repair including potential regeneration indices. Post-MI mice (GRK2 KO, βARKct mice and wild-type and non-transgenic control mice) were treated with 5-ethynyl-2’-deoxyuridine (EdU) or Bromodeoxyuridine (BrDU) to examine indices of DNA proliferation in myocytes as well as Ki67 staining. We also quantitated c-kit+ cells and myocytes in the post-MI hearts to compare how either loss of GRK2 expression or inhibition via its C-terminus altered potential regeneration mechanisms compared to control mice with endogenous GRK2 levels and activity. We found significantly more BrDU positive myocytes in post-MI hearts with lower GRK2 and this correlated with increased myocytes that were also cKit+. Thus, it appears that the myocardial functional improvement seen in the post-MI heart with targeted lowering of GRK2 involves, to at least a certain extent, regenerative mechanisms. This adds novel insight into the therapeutic potential of GRK2 inhibition for HF.

215 INVESTIGATION OF A PREFERENTIALLY UPREGULATED GENE CLUSTER IN DAY 7 BOVINE EMBRYOS DERIVED FROM RNA SEQUENCING DATA

2013 ◽  
Vol 25 (1) ◽  
pp. 256 ◽  
Author(s):  
A. Al Naib ◽  
S. Mamo ◽  
P. Lonergan
Keyword(s):  
Rna Sequencing ◽  
Mature Oocyte ◽  
Blastocyst Stage ◽  
Blastocyst Formation ◽  
Sequencing Data ◽  
Cell Stage ◽  
Uterine Endometrium ◽  
Embryonic Origin

Successful establishment and maintenance of pregnancy requires optimum conceptus-maternal cross talk. Despite significant progress in our understanding of the temporal changes in the transcriptome of the uterine endometrium, we have only a rudimentary knowledge of the genes and pathways governing growth and development of the bovine conceptus. A recent RNA sequencing study from our group (Mamo et al. 2011 Biol. Reprod. 85, 1143–1151) described the global transcriptome profile of the bovine conceptus at 5 key stages of its pre- and peri-implantation growth (Days 7, 10, 13, 16, and 19) using RNA sequencing techniques. One cluster of genes (n = 1680 transcripts) was preferentially upregulated at Day 7 and subsequently downregulated, suggesting that these genes might be markers of blastocyst formation. The objective of this study was to characterise the pattern of expression of these genes before Day 7 (i.e. from the zygote to blastocyst stage). The list of genes was submitted to DAVID (Database for Annotation, Visualisation, and Integrated Discovery) to take advantage of available ontology information contained therein. The expression of 9 genes belonging to ontologies specifically related to embryo developmental (GINS1, TAF8, ESRRB, NCAPG2, SP1, XAB2, CDC2L1, MSX1, and AQP3) plus Na/K ATPase, a gene previously known to be involved in blastocoe formation, was studied by quantitative real-time PCR (QPCR) in 6 replicate pools of 5 embryos produced by maturation, fertilization, and embryo culture in vitro. Stages studies included immature and mature oocyte, zygote, 2- cell, 4-cell, 8-cell, 16-cell, morula, blastocyst, and hatched blastocyst. In addition, in vivo derived Day 13 and Day 16 embryos were included as controls to confirm down-regulation after Day 7. Data were analysed using the GLM procedure of SAS. The QPCR expression data supported the RNA Seq data in that expression of all transcripts was downregulated after the blastocyst stage. Expression before the blastocyst stage was characterised by 1 of 3 broad patterns: (1) the expression was of maternal origin where the expression was very high up to 8-cell stage and decreased subsequently (MSX1), (2) the expression was of embryonic origin being low up to the 8-cell stage and increasing thereafter (TAF8, ESRRB, AQP3, and Na/K ATPase), or (3) static or decreased expression from oocyte to the maternal-zygotic transition followed by increased expression from the 16-cell stage (GINS1, NCAPG2, SP1, XAB2, and CDC2L1). In conclusion, the genes identified in this cluster, despite having different patterns of expression before the blastocyst stage, may represent markers of blastocyst formation in cattle given their downregulation subsequently. Supported by Science Foundation Ireland (07/SRC/B1156).

Abstract 293: MicroRNA-125b-5p Protect the Mouse Heart from Ischemic Injury by Repressing Pro-apoptotic Bak1 And Klf13 in Cardiomyocytes

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Zuzana Broskova ◽  
Kyoung-mi Park ◽  
Yongchao Wang ◽  
Il-man Kim
Keyword(s):  
Target Genes ◽  
Cardiac Injury ◽  
Ischemic Injury ◽  
Mouse Heart ◽  
Loss Of Function ◽  
Increased Sensitivity ◽  
Induced Apoptosis ◽  
End Stage ◽  
And Function

Cardiac injury is accompanied by dynamic changes in the expression of microRNAs (miRs), small non-coding RNAs that post-transcriptionally regulate target genes. For example, miR-125a is up-regulated in patients with heart failure (HF), while miR-125b is down-regulated in patients with end-stage dilated cardiomyopathy (DCM) and ischemic DCM. Circulating levels of these two miRs have been recently proposed as potential biomarkers of HF. We previously showed that β1-adrenergic receptor-mediated cardioprotective signaling through β-arrestin1 stimulates the processing of miR-125a and miR-125b in mouse heart (Figure A-C). Here, we hypothesize that these two miRs might confer cardioprotection against ischemic injury. Using cultured cardiomyocyte (CM) and in vivo approaches, we show that these miRs are ischemic stress-responsive protectors against CM apoptosis. CMs lacking miR-125a or miR-125b have an increased sensitivity to stress-induced apoptosis, while CMs overexpressing miR-125a or miR-125b have increased phospho-AKT pro-survival signaling. Moreover, we demonstrate that loss-of-function of miR-125b in mouse heart causes abnormalities in cardiac structure and function after myocardial infarction. The cardioprotective roles of the two miRs during ischemic injury are in part attributed to direct repression of the pro-apoptotic genes Bak1 and Klf13 in CMs (Figure D). In conclusion, these findings reveal pivotal roles for miR-125a and miR-125b as important regulators of CM survival during cardiac injury.

Abstract 127: Mode of Injury Affects the Course of Regeneration and Repair in Neonatal and Adult Mouse Heart

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Tal Konfino ◽  
Natalie Landa-Rouben ◽  
Jonathan Leor
Keyword(s):  
Granulation Tissue ◽  
Adult Mouse ◽  
Cardiac Injury ◽  
Cardiac Regeneration ◽  
Lv Function ◽  
Mouse Heart ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Newborn Mice ◽  
Adult Mice

PURPOSE: Recent reports have demonstrated complete cardiac regeneration in newborn mice following resection of the cardiac apex. However, different types of injury could affect the mechanism of regeneration and repair. HYPOTHESIS: We aimed to test the hypothesis that the course of repair and regeneration after MI is different from apical resection in both neonatal and adult mouse heart. Methods and Results: Apical resection or permanent LAD coronary artery ligation was induced in 1-day-old or 12-week-old ICR mice. Echocardiography was used to confirm and monitor cardiac injury and remodeling. Mice were euthanized at different time points after operation, and hearts were harvested, processed, immunostained and compared with sham operated neonatal and adult hearts. Histological and immunohistochemical examination of both resected and infarcted neonatal hearts revealed inflammation and granulation tissue formation within 3 to 5 days. In the resected hearts, early regeneration was identified at the injured sites, and marked dedifferentiation of cardiomyocytes, represented by sarcomeric disassembly and marginalization, was evident around the injured areas. In addition, we noticed intensive proliferation of young cardiomyocytes which infiltrated the granulation tissue and formed a new myocardium within 21 days. In contrast, incomplete regeneration with residual small infract was detected 28 days after coronary occlusion. Echocardiography at 2,7,14 and 28 days after MI confirmed deteriorating LV function and LV remodeling with apical aneurysm formation. Surprisingly, 21 days after cardiac injury in adult mice, MI produced typical, thin, fibrotic scar whereas apical resection produced an apical tumor-like thick scar. Conclusions: The mode of injury, whether resection or infarction, affect regeneration and repair in both neonatal and adult mouse heart. Particularly, after apical resection, the newborn heart almost completely regenerates whereas regeneration is incomplete after MI, suggesting that infarction and subsequent inflammation might inhibit complete regeneration. Understanding these differences could be translated to development of new approaches to induce myocardial regeneration in adult heart.

Abstract 277: MicroRNA-125a-5p Protects the Mouse Heart From Ischemic Injury by Repressing Pro-apoptotic Bak1 and Klf13 in Cardiomyocytes

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Bruno Moukette ◽  
Tatsuya Aonuma ◽  
Il-man Kim
Keyword(s):  
Target Genes ◽  
Cardiac Injury ◽  
Cell Types ◽  
Mouse Heart ◽  
Small Noncoding Rnas ◽  
Increased Sensitivity ◽  
Β Blocker ◽  
Apoptotic Genes

Background: Cardiac injury is accompanied by dynamic changes in the expression of microRNAs (miRs), which are small noncoding RNAs to downregulate target genes. MiR-125a-5p (miR-125a) is downregulated in patients with myocardial infarction (MI). We reported that miR-125a is upregulated by the β-blocker carvedilol (Carv) acting through β-arrestin1-biased β1-adrenergic receptor (β1AR; receptor found mainly in cardiomyocytes [CMs]) cardioprotective signaling (Figure A). We also showed that pro-apoptotic genes bak1 and klf13 are downregulated by Carv and are upregulated after MI. Here, we hypothesize that miR-125a in CMs favorably regulates cardiac functional and structural remodeling after MI by repressing bak1 and klf13. Methods and Results: Fractionation of cardiac cell types from heart tissues reveals that the expression of miR-125a is higher in CMs than other myocardial cells. Using cultured CM and in vivo approaches, we show that miR-125a is an ischemic stress-responsive protector against CM apoptosis. CMs lacking miR-125a exhibit an increased sensitivity to apoptosis, while CMs overexpressing miR-125a have increased phospho-AKT pro-survival signaling. Moreover, we show that miR-125a is downregulated in post-MI mouse hearts and miR-125a overexpression protects mouse hearts against MI. We also show that global genetic deletion of miR-125a in mice worsens maladaptive post-MI remodeling. Mechanistically, the cardioprotective role of miR-125a during MI is in part attributed to direct repression of the pro-apoptotic genes bak1 and klf13 in CMs (Figure B). Conclusions: These findings reveal a pivotal role for miR-125a in regulating CM survival during MI.

scholarly journals Expandable human cardiovascular progenitors from stem cells for regenerating mouse heart after myocardial infarction

2019 ◽  
Vol 116 (3) ◽  
pp. 545-553 ◽  
Author(s):  
Verena Schwach ◽  
Maria Gomes Fernandes ◽  
Saskia Maas ◽  
Sophie Gerhardt ◽  
Roula Tsonaka ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Growth Factor ◽  
Mouse Model ◽  
High Efficiency ◽  
Left Ventricular ◽  
Cardiac Repair ◽  
Mouse Heart ◽  
Cell Renewal ◽  
The Impact

Abstract Aims Cardiovascular diseases caused by loss of functional cardiomyocytes (CMs) are a major cause of mortality and morbidity worldwide due in part to the low regenerative capacity of the adult human heart. Human pluripotent stem cell (hPSC)-derived cardiovascular progenitor cells (CPCs) are a potential cell source for cardiac repair. The aim of this study was to examine the impact of extensive remuscularization and coincident revascularization on cardiac remodelling and function in a mouse model of myocardial infarction (MI) by transplanting doxycycline (DOX)-inducible (Tet-On-MYC) hPSC-derived CPCs in vivo and inducing proliferation and cardiovascular differentiation in a drug-regulated manner. Methods and results CPCs were injected firstly at a non-cardiac site in Matrigel suspension under the skin of immunocompromised mice to assess their commitment to the cardiovascular lineage and ability to self-renew or differentiate in vivo when instructed by systemically delivered factors including DOX and basic fibroblast growth factor (bFGF). CPCs in Matrigel were then injected intra-myocardially in mice subjected to MI to assess whether expandable CPCs could mediate cardiac repair. Transplanted CPCs expanded robustly both subcutis and in the myocardium using the same DOX/growth factor inducing regime. Upon withdrawal of these cell-renewal factors, CPCs differentiated with high efficiency at both sites into the major cardiac lineages including CMs, endothelial cells, and smooth muscle cells. After MI, engraftment of CPCs in the heart significantly reduced fibrosis in the infarcted area and prevented left ventricular remodelling, although cardiac function determined by magnetic resonance imaging was unaltered. Conclusion Replacement of large areas of muscle may be required to regenerate the heart of patients following MI. Our human/mouse model demonstrated that proliferating hPSC-CPCs could reduce infarct size and fibrosis resulting in formation of large grafts. Importantly, the results suggested that expanding transplanted cells in situ at the progenitor stage maybe be an effective alternative causing less tissue damage than injection of very large numbers of CMs.

scholarly journals Direct Cardiac Reprogramming: Advances in Cardiac Regeneration

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Olivia Chen ◽  
Li Qian
Keyword(s):  
Myocardial Infarction ◽  
Heart Disease ◽  
Cell Fate ◽  
Early Stage ◽  
Cardiac Injury ◽  
Cardiac Regeneration ◽  
Scar Tissue ◽  
Coronary Events

Heart disease is one of the lead causes of death worldwide. Many forms of heart disease, including myocardial infarction and pressure-loading cardiomyopathies, result in irreversible cardiomyocyte death. Activated fibroblasts respond to cardiac injury by forming scar tissue, but ultimately this response fails to restore cardiac function. Unfortunately, the human heart has little regenerative ability and long-term outcomes following acute coronary events often include chronic and end-stage heart failure. Building upon years of research aimed at restoring functional cardiomyocytes, recent advances have been made in the direct reprogramming of fibroblasts toward a cardiomyocyte cell fate bothin vitroandin vivo. Several experiments show functional improvements in mouse models of myocardial infarction followingin situgeneration of cardiomyocyte-like cells from endogenous fibroblasts. Though many of these studies are in an early stage, this nascent technology holds promise for future applications in regenerative medicine. In this review, we discuss the history, progress, methods, challenges, and future directions of direct cardiac reprogramming.

scholarly journals Osteocrin, a novel myokine, prevents diabetic cardiomyopathy via restoring proteasomal activity

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Xin Zhang ◽  
Can Hu ◽  
Xiao-Pin Yuan ◽  
Yu-Pei Yuan ◽  
Peng Song ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Injury ◽  
Neonatal Rat ◽  
Protective Effects ◽  
Rat Cardiomyocytes ◽  
Proteasomal Activity ◽  
Virus Serotype

AbstractProteasomal activity is compromised in diabetic hearts that contributes to proteotoxic stresses and cardiac dysfunction. Osteocrin (OSTN) acts as a novel exercise-responsive myokine and is implicated in various cardiac diseases. Herein, we aim to investigate the role and underlying molecular basis of OSTN in diabetic cardiomyopathy (DCM). Mice received a single intravenous injection of the cardiotrophic adeno-associated virus serotype 9 to overexpress OSTN in the heart and then were exposed to intraperitoneal injections of streptozotocin (STZ, 50 mg/kg) for consecutive 5 days to generate diabetic models. Neonatal rat cardiomyocytes were isolated and stimulated with high glucose to verify the role of OSTN in vitro. OSTN expression was reduced by protein kinase B/forkhead box O1 dephosphorylation in diabetic hearts, while its overexpression significantly attenuated cardiac injury and dysfunction in mice with STZ treatment. Besides, OSTN incubation prevented, whereas OSTN silence aggravated cardiomyocyte apoptosis and injury upon hyperglycemic stimulation in vitro. Mechanistically, OSTN treatment restored protein kinase G (PKG)-dependent proteasomal function, and PKG or proteasome inhibition abrogated the protective effects of OSTN in vivo and in vitro. Furthermore, OSTN replenishment was sufficient to prevent the progression of pre-established DCM and had synergistic cardioprotection with sildenafil. OSTN protects against DCM via restoring PKG-dependent proteasomal activity and it is a promising therapeutic target to treat DCM.

Abstract 218: Cardiac Side Population Cells Give Rise to Cardiomyocytes in the Adult Heart

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Amritha Yellamilli ◽  
Ingrid Bender ◽  
Yi Ren ◽  
Jop H van Berlo
Keyword(s):  
Mouse Model ◽  
Progenitor Cells ◽  
Side Population ◽  
Cardiac Injury ◽  
Cardiac Regeneration ◽  
Tamoxifen Treatment ◽  
Side Population Cells ◽  
Adult Heart ◽  
Chase Period

Therapies that enhance cardiac regeneration have the potential to improve heart failure outcomes. One strategy to enhance cardiac regeneration is by activating endogenous cardiac progenitor cells. Cardiac side population cells (cSPCs) are proposed progenitor cells that reside in the heart; however, their putative progenitor cell properties are based on cell culture data and transplantation studies performed with isolated cSPCs. To determine the endogenous regenerative potential of cSPCs in vivo , we generated a mouse model that harbors an Abcg2-driven, tamoxifen-inducible Cre recombinase and crossed it to a GFP reporter mice. One month after tamoxifen treatment, we obtained efficient GFP-labeling of side population cells with 47.0 ± 11.05% of bone marrow side population cells and 75.8 ± 10.87% of cSPCs. Importantly, during a one-month chase period, we observed a three-fold increase in GFP-labeled cardiomyocytes when compared to a 1-week chase period. We quantified the extent of GFP-labeling of cardiomyocytes using adult cardiomyocyte isolation, where we measured 0.8% GFP labeled cardiomyocytes after a one-month chase period. We also observed labeling of many other cell types in the heart, such as endothelial cells, smooth muscle cells, and pericytes. We are currently testing to what extent cardiac injury enhances cSPC derived cardiomyocyte formation. Using our mouse model that efficiently labels side population cells in vivo , we demonstrated that cSPCs contribute cardiomyocytes in the adult heart in vivo .

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