Abstract 242: Subcutaneous and Visceral Adipose-Derived Stem Cells Have Similar Biological Properties and Both Improve Cardiac Function of Infarcted Rat Hearts

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Chao Chi ◽  
Bo Xiang ◽  
Jixian Deng ◽  
Fei Wang ◽  
Kanmani Natarajan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cardiac Function ◽  
Formation Rate ◽  
Biological Properties ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Ventricular Ejection Fraction ◽  
Visceral Adipose

Background: Adipose stem cells (ASC) from subcutaneous and visceral adipose tissues have been studied individually. However, it is unclear whether ASC from the two sources have different biological properties and, more importantly, whether one sub-type of ASC is more effective in treatment of CHF. This study was designed to address these concerns. Methods: Morphology, yield, proliferation, surface markers, and cytokine secretion of rat subcutaneous ASC (S-ASC) and visceral ASC (V-ASC) were analyzed. A rat model of myocardial infarction (MI) was established by occlusion of the LAD. 7 days after MI, S-ASC (n = 11), V-ASC (n = 11), and cell culture medium (Control, n = 7) were injected into the infarct rim, respectively. Cardiac function of the infarcted hearts was monitored with MRI for 6 months. Results: Both S-ASC and V-ASC exhibited a fibroblast-like morphology and expressed stromal cell markers (CD29, CD90 and CD105). No significant expression of hematopoietic markers (CD11b, CD34 and CD45) was found. Under appropriate conditions, both cells could differentiate to adipocyte- and osteocyte-like cells. Both of them expressed a significant level of HGF, IGF-1 and VEGF. As to their differences, V-ASC had approximately 3-times greater cell yield and a lower colony-formation rate (9.8±1.0% vs.13.5±2.6%) relative to S-ASC. In contrast, S-ASC showed a significantly greater growth rate (Doubling Time: 17.9 h vs. 26.0 h) relative to V-ASC. Both S-ASC and V-ASC-treated hearts showed a significantly greater left ventricular ejection fraction (LVEF, 58.3% and 56.7%) than the control group (LVEF, 47.2%) at end of 6 months. LVEF between the two ASC-treated groups was not significantly different. Finally, the implanted stem cells were readily detected in vivo with MRI for at least 6 months. Myocardial tissue sections showed existence of ASC and their locations matched with MRI signals. Conclusions: S-ASC and V-ASC share several biological characteristics. Both provide comparable significant improvement on cardiac function. Moreover, these implanted cells can be reliably tracked for at least 6 months using MRI. We conclude that the S-ASC and V-ASC are equally effective for treatment of heart failure.

P5397Mesenchymal stem cells derived from bone marrow promotes cardiomyocytes survival under hypoxia through exosomal miR-210

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Cheng ◽  
X Y Song ◽  
L Chen ◽  
R D Xu ◽  
Q Qin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Bone Marrow ◽  
Cardiac Function ◽  
Conditioned Medium ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Ventricular Ejection Fraction ◽  
Paracrine Effect

Abstract Mesenchymal stem cells derived from bone marrow promotes cardiomyocytes survival under hypoxia through exosomal miR-210 Background A paracrine effect was regarded as the key mechanism involved in the MSC (mesenchymal stem cell)-based treatment for myocardial infarction. In our pilot experiments, hypoxia remarkably promotes MSC to paracrine exosomal miR-210, which could significantly enhance the cardiomyocytes survival in hypoxic incubation, suggesting that exosomal miR-210 played critical roles in the favorable paracrine effect of MSC on cardiomyocytes. Purpose The aim of this study was to investigate the important mechanism by which MSCs promote the tolerance of cardiomyocytes to hypoxia by secreting exosomal miR-210. Methods and results The exosomes were isolated from MSCs conditioned medium through ultracentrifugation, and we detected that miR-210 was the most abundant in MSC-exosome and increased most prominently in the hypoxia. The extracted exosomes were prepared for conditioned medium and the effect on myocardial protection was examined. The viability of control group was much better than the cardiomyocytes treated with hypoxia, but it was further increased in the presence of MSC-exosome, however, measurement was significantly lower in cardiomyocytes in hypoxia with exosomes derived from MSCs treated with GW4869. Subsequently, the co-localization of miR-210 with exosome-specific surface markers CD81 and CD63 were observed by immunofluorescence technique. Continuous magnetic live cell imaging was used to observe the uptake of exosome by cardiomyocytes, and fluorescence localization was used to observe the localization of miR-210 with Cy3 fluorescence in cardiomyocytes. Then, we demonstrated that MSCs exosomal miR-210 exerts the cardioprotective effect by regulating the AIFM3 (apoptosis-inducing factor mitochondria-associated protein 3), and we directly overexpressed miRNA-210 in cardiomyocytes and the results showed that the regulatory activity of the intake of exosomal miR-210 was consistent with that of the biological exosomal miR-210. Finally, we verified the protective effect on the ischemic myocardium by constructing rat myocardial infarction models. The level of apoptosis was detected at 1 week after myocardial infarction. The left ventricular ejection fraction and ventricular remodeling were measured at 4 weeks. In vivo, we demonstrated that explanted miR-210 from transplanted MSCs significantly reduced myocardial necrosis and apoptosis induced by ischemia and improved cardiac function and myocardial remodeling. Conclusion Here, we show that the exosomal miR-210 secreted by MSCs significantly increase the viability of cardiomyocytes and cardiac function. These findings suggest that exosomal miR-210 is a key effector that mediates the protection against hypoxia. Acknowledgement/Funding National Natural Science Foundation of China (Grant Nos. 81470467)

scholarly journals Recovery of Infarcted Myocardium in an In Vivo Experiment

Medicina ◽  
2011 ◽  
Vol 47 (11) ◽  
pp. 88 ◽  
Author(s):  
Raimondas Širmenis ◽  
Antanas Kraniauskas ◽  
Rasa Jarašienė ◽  
Daiva Baltriukienė ◽  
Audronė Kalvelytė ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Function ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Infarcted Myocardium ◽  
Myogenic Stem Cells

Acute myocardial infarction leads to the loss of functional cardiomyocytes and structural integrity. The adult heart cannot repair the damaged tissue due to inability of mature cardiomyocytes to divide and lack of stem cells. The aim of this study was to evaluate the efficiency of introduced autologous skeletal musclederived stem cells to recover the function of acutely infarcted rabbit heart in the early postoperative period. Material and Methods. As a model for myocardium restoration in vivo, experimental rabbit heart infarct was used. Autologic adult myogenic stem cells were isolated from skeletal muscle and propagated in culture. Before transplantation, the cells were labeled with 4´,6-diamidino-2-phenylindole and then, during heart surgery, introduced into the rabbit acutely infarcted myocardium. Postoperative cardiac function was monitored by recording electrocardiograms and echocardiograms. At the end of the experiment, the efficiency of cell integration was evaluated histologically. Results. Rabbit cardiac function recovered after 1 month after the induction of experimental infarction both in the control and experimental groups. Therefore, the first month after the infarction was the most significant for the assessment of cell transplantation efficacy. Transplanted cell integration into infarcted myocardium was time- and individual-dependent. Evaluation of changes in left ventricular ejection fraction after the induction of myocardial infarction revealed better recovery in the experimental group; however, the difference among animals in the experimental and control groups varied and was not significant. Conclusions. Autologous myogenic stem cells repopulated infarcted myocardium with different efficiency in each individual. This variability may account for the observed difference in postoperative cardiac recovery in a rabbit model.

scholarly journals A Randomized Controlled Trial to Study the Effect of Yoga Therapy on Cardiac Function and N Terminal Pro BNP in Heart Failure

2014 ◽  
Vol 9 ◽  
pp. IMI.S13939 ◽  
Author(s):  
Bandi Hari Krishna ◽  
Pravati Pal ◽  
G. K. Pal ◽  
J. Balachander ◽  
E. Jayasettiaseelon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Medical Therapy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Tei Index ◽  
Ventricular Ejection Fraction ◽  
Yoga Therapy ◽  
Standard Medical Therapy

Aims The purpose of this study was to evaluate whether yoga training in addition to standard medical therapy can improve cardiac function and reduce N terminal pro B-type natriuretic peptide (NT pro BNP) in heart failure (HF). Methods 130 patients were recruited and randomized into two groups: Control Group (CG) ( n = 65), Yoga Group (YG). In YG, 44 patients and in CG, 48 patients completed the study. Cardiac function using left ventricular ejection fraction (LVEF), myocardial performance index (Tei index), and NT pro BNP, a biomarker of HF, was assessed at baseline and after 12 weeks. Result Improvement in LVEF, Tei index, and NT pro BNP were statistically significant in both the groups. Furthermore, when the changes in before and after 12 weeks were in percentage, LVEF increased 36.88% in the YG and 16.9% in the CG, Tei index was reduced 27.87% in the YG and 2.79% in the CG, NT pro BNP was reduced 63.75% in the YG and 10.77% in the CG. The between group comparisons from pre to post 12 weeks were significant for YG improvements (LVEF, P < 0.01, Tei index, P < 0.01, NT pro BNP, P < 0.01). Conclusion These results indicate that the addition of yoga therapy to standard medical therapy for HF patients has a markedly better effect on cardiac function and reduced myocardial stress measured using NT pro BNP in patients with stable HF.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

1999 ◽  
Vol 77 (7) ◽  
pp. 510-519 ◽  
Author(s):  
Katherine M Kavanagh ◽  
Patricia A Guerrero ◽  
Bodh I Jugdutt ◽  
Francis X Witkowski ◽  
Jeffrey E Saffitz
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Dysfunction ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Functional Abnormality ◽  
Ventricular Ejection Fraction ◽  
Anisotropic Properties

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

scholarly journals Bone marrow-derived stromal cells home to and remain in the infarcted rat heart but fail to improve function: an in vivo cine-MRI study

2008 ◽  
Vol 295 (2) ◽  
pp. H533-H542 ◽  
Author(s):  
Carolyn A. Carr ◽  
Daniel J. Stuckey ◽  
Louise Tatton ◽  
Damian J. Tyler ◽  
Sarah J. M. Hale ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Therapy ◽  
Cardiac Function ◽  
Stromal Cells ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cine Mri ◽  
Iron Oxide Particles ◽  
Ventricular Ejection Fraction

Basic and clinical studies have shown that bone marrow cell therapy can improve cardiac function following infarction. In experimental animals, reported stem cell-mediated changes range from no measurable improvement to the complete restoration of function. In the clinic, however, the average improvement in left ventricular ejection fraction is around 2% to 3%. A possible explanation for the discrepancy between basic and clinical results is that few basic studies have used the magnetic resonance (MR) imaging (MRI) methods that were used in clinical trials for measuring cardiac function. Consequently, we employed cine-MR to determine the effect of bone marrow stromal cells (BMSCs) on cardiac function in rats. Cultured rat BMSCs were characterized using flow cytometry and labeled with iron oxide particles and a fluorescent marker to allow in vivo cell tracking and ex vivo cell identification, respectively. Neither label affected in vitro cell proliferation or differentiation. Rat hearts were infarcted, and BMSCs or control media were injected into the infarct periphery ( n = 34) or infused systemically ( n = 30). MRI was used to measure cardiac morphology and function and to determine cell distribution for 10 wk after infarction and cell therapy. In vivo MRI, histology, and cell reisolation confirmed successful BMSC delivery and retention within the myocardium throughout the experiment. However, no significant improvement in any measure of cardiac function was observed at any time. We conclude that cultured BMSCs are not the optimal cell population to treat the infarcted heart.

Abstract 14195: Impact of Leukocyte Filtration and Leukocyte Modulation on Recovery of Heart Function After Prolonged Cardiac Arrest Treated With ECPR in a Porcine Model

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Jensyn VanZalen ◽  
Takahiro Nakashima ◽  
Annie Phillips ◽  
Joseph Hill ◽  
Alyssa Enciso ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiac Function ◽  
Heart Function ◽  
Randomized Study ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Swine Model ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Ventricular Ejection Fraction

Background: Extracorporeal cardiopulmonary resuscitation (ECPR) improves survival of patients with prolonged cardiac arrest (CA) that is refractory to standard CPR and ACLS. It has been proposed that ECPR accentuates inflammation after CA, potentially limiting its effectiveness. The benefits of leukocyte filters or leukocyte-modulating devices in conjunction with ECPR have not been studied. Hypothesis: When paired with ECPR, inflammation-modulating devices targeting leukocytes may improve recovery of cardiac function after prolonged cardiac arrest. Methods: In a randomized study, 24 swine (40±5kg) underwent 8min of untreated ventricular fibrillation CA followed by CPR with mechanical chest compressions and impedance threshold device for 30 min (total arrest time = 38min), immediately followed by 8h of ECPR with heparin anticoagulation and temperature maintained at 33°C. Group 1 (n=8) had standard ECPR system (control), Group 2 (n=8) had a leukocyte filter device (LF) added to the ECPR circuit, an and Group 3 (n=8) had a leukocyte modulation device (LMOD) added to the ECPR circuit. Recovery of cardiac function was measured using a cardiac resuscitablity score (CRS) and left ventricular ejection fraction (LVEF) via transthoracic echocardiography. Data was collected at baseline (prior CA) and after 8h of ECPR. Data analysis: single-factor ANOVA test (p<0.05 significance). Results: There were no statically significant differences between the groups in CRS (Control = 3.3 ± 2.4, LF = 4.0 ± 2.8, LMOD = 2.1 ± 2.6; p=0.37) or LVEF (Control = 59% ± 27%, LF = 49% ± 29% LMOD = 34% ± 38%: p=0.34) at 8 hours after ECPR initiation (Table 1). Discussion: In this swine model of prolonged cardiac arrest treated with ECPR, addition of a leukocyte filter or leukocyte modulation device to the ECPR circuit did not improve recovery of cardiac function during the first 8 hours after initiating ECPR.

scholarly journals Sustained subcutaneous delivery of secretome of human cardiac stem cells promotes cardiac repair following myocardial infarction

2020 ◽  
Author(s):  
Andrew R Kompa ◽  
David W Greening ◽  
Anne M Kong ◽  
Paul J McMillan ◽  
Haoyun Fang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Function ◽  
Extracellular Vesicles ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Stem Cells ◽  
Subcutaneous Implantation ◽  
Ventricular Ejection Fraction ◽  
Post Implantation

Abstract Aims To establish pre-clinical proof of concept that sustained subcutaneous delivery of the secretome of human cardiac stem cells (CSCs) can be achieved in vivo to produce significant cardioreparative outcomes in the setting of myocardial infarction. Methods and results Rats were subjected to permanent ligation of left anterior descending coronary artery and randomized to receive subcutaneous implantation of TheraCyte devices containing either culture media as control or 1 × 106 human W8B2+ CSCs, immediately following myocardial ischaemia. At 4 weeks following myocardial infarction, rats treated with W8B2+ CSCs encapsulated within the TheraCyte device showed preserved left ventricular ejection fraction. The preservation of cardiac function was accompanied by reduced fibrotic scar tissue, interstitial fibrosis, cardiomyocyte hypertrophy, as well as increased myocardial vascular density. Histological analysis of the TheraCyte devices harvested at 4 weeks post-implantation demonstrated survival of human W8B2+ CSCs within the devices, and the outer membrane was highly vascularized by host blood vessels. Using CSCs expressing plasma membrane reporters, extracellular vesicles of W8B2+ CSCs were found to be transferred to the heart and other organs at 4 weeks post-implantation. Furthermore, mass spectrometry-based proteomic profiling of extracellular vesicles of W8B2+ CSCs identified proteins implicated in inflammation, immunoregulation, cell survival, angiogenesis, as well as tissue remodelling and fibrosis that could mediate the cardioreparative effects of secretome of human W8B2+ CSCs. Conclusions Subcutaneous implantation of TheraCyte devices encapsulating human W8B2+ CSCs attenuated adverse cardiac remodelling and preserved cardiac function following myocardial infarction. The TheraCyte device can be employed to deliver stem cells in a minimally invasive manner for effective secretome-based cardiac therapy.

Abstract 209: Ketone Bodies Ameliorate Cardiac Function in Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Jessica Gambardella ◽  
Marco B. Morelli ◽  
Xujun Wang ◽  
Gaetano Santulli
Keyword(s):  
Cardiac Function ◽  
Ketone Bodies ◽  
Left Ventricular ◽  
Cardiac Cells ◽  
Left Ventricular Ejection ◽  
Standard Diet ◽  
Apoptotic Pathway ◽  
Ventricular Ejection Fraction ◽  
Cardiac Phenotype

Background: Beta hydroxibutirrate (BHB) is the main ketone body produced during fasting or carbohydrate deprivation as an alternative fuel. Mounting evidence suggests that after myocardial infarction (MI), the mitochondrial impairment and metabolic failure coincide with increased levels and utilization of BHB. However, whether the BHB increase is adaptive or maladaptive in damaged myocardium, has never been evaluated. Aim: Our scope was to explore the effects of BHB on cardiac function after ischemia both in vivo and in vitro . Methods and Results: In cultured cardiomyoblasts, the administration of BHB (3 mMol) reduces the activation of caspase-3 in response to ischemia, as well as the number of tunnel positive nuclei. Specifically, the mitochondrial apoptotic pathway seems affected, as BHB reduces cytochrome-C release induced by ischemia. Mitochondrial structure and interconnections, soundly affected by ischemia, were significantly retained in presence of BHB, as well as mitochondrial membrane potential (assessed via TMRE). The preserved mitochondrial health was further supported by higher levels of PGC1-alpha detected in cells exposed to ischemia plus BHB compared to ischemia alone. To explore the in vivo effects of BHB on ischemia damaged- myocardium, we administrated carbohydrate-null diet ( ketogenic diet , KD) or standard diet-supplemented with BHB, to post-MI mice. Both groups treated with KD and BHB supplemented diet displayed preserved left ventricular ejection fraction respect to untreated infarcted mice. The protective effects of BHB on cardiac phenotype were mirrored by increased levels of PGC1-alpha in the myocardium of treated mice, in terms of protein and transcription levels. Interestingly, in the hearts of mice fed KD and BHB supplemented diet, we observed a marked difference in histone acetylation pattern. Conclusions: BHB protects cardiac cells from apoptotic and mitochondrial damage induced by ischemia. Through its ability to regulate epigenetic modifications, BHB could activate a gene expression program able to support mitochondrial function, thereby representing a powerful therapeutic strategy.

scholarly journals Effect of Traditional Chinese Medicine Poge Heart-Saving Decoction on Cardiac Function in Heart Failure Rat Model

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Lei Liu ◽  
Yanfei Mo ◽  
Bingying Wu ◽  
Zongliang Yu ◽  
Bugao Sun
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Sham Group ◽  
Test Group ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Blank Control Group ◽  
Ventricular Ejection Fraction

Background. Poge heart-saving decoction (PHSD) has been used as a medicine treating heart failure in China for many years. The study aimed to explore the effect of PHSD on cardiac function in heart failure conditions and its underlying mechanism. Methods. Adriamycin was used to induce the model of heart failure (HF) in rats. Sixty rats were randomly divided into six groups: blank control group, sham group, 9.33 g/kg group (low-PHSD, test group), 13.995 g/kg group (moderate-PHSD, test group), 18.66 g/kg group (high-PHSD, test group), and fosinopril group (4.67 mg/kg, comparison test group). Cardiac ultrasound was used to evaluate the cardiac function of the rats, and radioimmunoassay was used to measure aldosterone (ALD) and angiotensin II (AngII) levels in the serum. Results. Compared with the blank control group, the left ventricular end-diastolic dimension (LVEDd) and left ventricular end-systolic dimension (LVEDs) in the sham group were increased (1.04 ± 0.12 vs. 0.67 ± 0.13 cm; 0.75 ± 0.13 vs. 0.28 ± 0.10 cm; P < 0.05 ), and the left ventricular ejection fraction was decreased (36.65 ± 5.74 vs. 76.09 ± 4.23%; P < 0.05 ). The ejection fraction of HF rats was increased in 9.33 g/kg group, 13.995 g/kg group, and 18.66 g/kg group compared with those of the sham group (57.13 ± 1.63, 58.43 ± 1.98, and 59.21 ± 1.37 vs. 36.65 ± 5.74%; P < 0.05 ). PHSD also improved cardiac function by reducing the LVEDd and LVEDs (0.88 ± 0.11, 0.75 ± 0.13, and 0.72 ± 0.18 vs. 1.04 ± 0.12 cm; 0.62 ± 0.10, 0.63 ± 0.17, and 0.45 ± 0.11 vs. 0.75 ± 0.13 cm; P < 0.05 ). The levels of ALD and AngII in the serum of rats in the sham group were significantly higher than those in the blank control group (371.58 ± 39.25 vs. 237.12 ± 17.35 μg/L; 232.18 ± 16.33 vs. 159.44 ± 18.42 pg/L; P < 0.05 ). The ALD and AngII of the rats in all of the three PHSD groups and the fosinopril group were decreased (276.81 ± 25.63, 277.18 ± 21.35, 268.19 ± 19.28, and 271.47 ± 28.96 vs. 371.58 ± 39.25 μg/L; 169.41 ± 27.53, 168.81 ± 19.78, 164.23 ± 21.34, and 174.27 ± 22.84 vs. 232.18 ± 16.33 pg/L; P < 0.05 ). The histopathological changes of the myocardium in the sham group showed the disorganized fiber, shaded staining, fracture, and zonation. The fracture of the myocardium was relieved in all groups except the sham group and the blank control group. Conclusion. Therefore, PHSD could shorten LVEDd and LVEDs of rats and reverse ventricular remodeling. The mechanism might be related to the inhibition of the activation level of renin-angiotensin-aldosterone system (especially ALD and AngII) and decreasing the postload of the heart.

scholarly journals The enhanced effect and underlying mechanisms of mesenchymal stem cells with IL-33 overexpression on myocardial infarction

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yueqiu Chen ◽  
Jianfeng Zuo ◽  
Weiqian Chen ◽  
Ziying Yang ◽  
Yanxia Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
Cardiac Function ◽  
Heart Function ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Therapeutic Effects ◽  
Ventricular Ejection Fraction

Abstract Background Interleukin 33 is known to have an important influence in the process of myocardial infarction, and the immunoregulatory function of MSCs could be influenced by cell factors. In this study, we evaluated the therapeutic efficacy of IL-33-overexpressing bone marrow mesenchymal stem cells (IL33-MSCs) on myocardial infarction (MI) and detected the inflammatory level and cardiac function in rats. Methods and results First, we evaluated the proliferation of T cells and polarization of macrophages that had been co-cultured with Vector-MSCs or IL33-MSCs. Co-culture experiments indicated that IL33-MSCs reduced T cell proliferation and enhanced CD206+ macrophage polarization. Second, we determined the inflammation level and cardiac function of PBS-, Vector-MSC-, and IL33-MSC-injected rats. Echocardiography indicated that left ventricular ejection fraction (LVEF) was enhanced in IL33-MSC-injected rats compared with Vector-MSC-injected rats. Postmortem analysis of rat heart tissue showed reduced fibrosis and less inflammation in IL33-MSC-injected rats. Conclusion These studies indicated that the IL33-MSC injection improved heart function and reduces inflammation in rats with MI compared with PBS or Vector-MSC injections. Graphical Abstract IL-33 overexpression enhances the immunomodulatory function and therapeutic effects of MSCs on acute MI via enhancing the polarization of macrophages toward M2, enhancing the differentiation of CD4+ T cells toward CD4+IL4+Th2 cells, and finally, reducing heart inflammation and enhancing heart function.

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