P2585Cardiac dysfunction after myocardial infarction: role of pro-inflammatory extracellular vesicles

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
V Biemmi ◽  
G Milano ◽  
A Ciullo ◽  
E Cervio ◽  
M Dei Cas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Extracellular Vesicles ◽  
Acute Phase ◽  
Troponin I ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Cytotoxic Effects

Abstract Background Myocardial infarction (MI) is associated with significant loss of cardiomyocytes (CM), which are replaced by a fibrotic scar. Necrotic CM release damage-associated proteins that stimulate innate immune pathways and macrophages (MΦ) tissue infiltration, which drives to the progression of inflammation and myocardial remodeling process. Both, loss of CM and inflammatory response are determinants of the long term ventricle remodeling and heart failure. Circulating inflammatory extracellular vesicles (EV) play a crucial role in the acute and chronic phases of MI, in terms of inflammatory progression. In this study we examined whether reducing the generation of inflammatory EV within few hours from the ischemic event may ameliorate cardiac outcome at short and long time-point in LAD rat model. Methods Before coronary artery ligation, rats were injected IP with a chemical inhibitor of neutral sphingomyelinase (nSMase) which is essential for the biogenesis and release of EVs. The number and size profile of plasma-derived EV was assessed by NTA analysis at baseline and 24hrs after MI. Multiple EV cytokine levels were simultaneously determined using enzyme-linked immunosorbent assay (ELISA)-based protein array technology. Heart global function was assessed by echocardiography and hemodynamic analysis performed at 7, 14 and 28 days after MI. Cytotoxic effects of circulating EV were evaluated ex-vivo in a Langedorff, system by measuring the level of cardiac troponin I (cTnI) in the perfusate. Mechanisms undergoing cytotoxic effects of EV derived from pro-inflammatory MΦ (MΦM1) were studied in vitro into primary rat neonatal CM. Results The induction of MI and the consequent inflammation, dramatically increase the number of circulating EV carrying inflammatory cytokines such as IL1α, ILβ and Rantes. Preventive inhibition nSMase significantly reduced the boost of inflammatory EV and cytokines in treated group as compared to control animals. The reduction of circulating EV post MI results in preserved LV ejection fraction at 7 and 28 days post-MI as compared to control group. Hemodynamic analysis confirmed functional recovery by displaying a higher velocity of LV relaxation and an improved contractility capacity in treated versus control group. The number of infiltrating CD68+ monocytes/macrophages in the infarct area was significantly reduced. Post-MI circulating EV induce cell death in adult CM when added to the perfusate of Langendorff, as assessed by the incresed level of cTnI into media. In vitro MΦM1-EV activated nuclear translocation of NF-kB. Specific inhibition of TLR4 receptor activity abrogated NF-kB translocation and reduced cell death. Indicating that the axis TRL4-NF-kB is essential in EV-mediated CM death. Conclusions Systemic inhibition of EV release during the acute phase of MI preserves heart function in an animal model of LAD. These findings suggest detrimental effects of exosomes in the acute phase of MI.

scholarly journals Effect of intramyocardial allogenic biomaterial injection on angiogenesis and postischemic scar remodeling in rats

2020 ◽  
Vol 22 (3) ◽  
pp. 156-166
Author(s):  
A. I. Lebedeva ◽  
S. A. Muslimov ◽  
L. A. Musina ◽  
E. M. Gareev ◽  
R. Z. Kadyrov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Acute Phase ◽  
Initial Period ◽  
Experimental Studies ◽  
Cytokine Expression ◽  
Control Group ◽  
Myocardial Inflammation ◽  
Coronary Artery Ligation ◽  
Statistical Research

Scar smoothing out, angiogenesis stimulation and cardiomyogenesis in myocardial infarction still remain pressing issues despite the variety of existing methods. One of the ways to correct them is intramyocardial implantation of an alloplant biomaterial (ABM) suspension. ABM serves as an inhibitor of fibroneogenesis in various tissues with chronic inflammatory processes. No studies have been carried out with regards to acute myocardial infarction. Objective: to assess the dynamics of the number of bFGF-1 + cells and CD68 macrophages, the degree of angiogenesis amidst the use of ABM in the formation of postinfarction scar in the experiment. Materials and methods. Experimental studies were performed on 100 male Wistar rats weighing 0.18–0.25 kg. Coronary artery ligation was performed on all animals. In the experimental group, the ABM suspension (12 mg) was injected intramyocardially. We used histological, electron microscopic, immunohistochemical (CD68, bFGF-1), morphometric and statistical research methods. Hearts were procured at day 3, 7, 14, 30, and 45. Results. The use of an allogeneic biomaterial immediately after coronary artery stenosis could reduce the area of cicatricial myocardial degeneration by two fold by accelerating inflammatory response and the onset of early proliferative phase. In the reactive zone after ABM implantation, macrophage myocardial infiltration significantly decreased in comparison to the control group. The use of ABM ensures significant predominance of bFGF-1+ cells in the initial period of inflammation (3–14 days). Subsequently (14–45 days), inflammatory cytokine expression became several times less, which corresponded to biodegradation and resorption of the biomaterial. In the control group, during the acute phase of inflammation (3–14 days), bFGF-1+ cells were low in number. Subsequently (14–45 days), cytokine expression increased significantly, causing rapid accumulation of collagen fibers and scarring. In myocardial regeneration after a heart attack in the experiment, ABM stimulated angiogenesis, whose level was three times higher than in the control group. It was noted that ABM serves as a regulator of the neofibrillogenesis-fibroclasia balance in tissue. Conclusion. Macrophage migration inhibition and suppression of pro-inflammatory orientation of macrophages should be indicated as one of the directions of therapeutic correction strategy for ischemic myocardial injuries. Alloplant biomaterial used in the acute phase of myocardial inflammation can serve as such alternative.

Abstract 192: Histological and Functional Assessment of Human Placental Stem Cells in an Induced Myocardial Infarction in Rats

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Georges Makhoul ◽  
Yu-Ting Ma ◽  
Minh Duong ◽  
Ray C J Chiu ◽  
Renzo Cecere
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Troponin I ◽  
Cardiac Cells ◽  
Coronary Artery Ligation ◽  
Regenerative Therapy ◽  
Age Related ◽  
Group 1

Purpose: Human bone marrow mesenchymal stem cells (hbmMSCs) have been studied extensively for myocardial regenerative therapy. However, such cells require invasive procreation and suffer from donor age-related declining quality. Recently, a more abundant resource of young MSCs has been isolated from an otherwise discarded organ: the human placenta mesenchymal stem cells (hpMSCs). In this study, we wanted to examine the survival, differentiation, and functionality of xenogeneic hpMSCs when implanted into an induced myocardial rat infarction. Methods: To inspect their stemness,hpMSCs underwent an In Vitro cardiac cell differentiation in a DMEM medium containing 5 Azacytidine. Additionally, hpMSCs were tested in a myocardial infarction animal model. Female Lewis rats (40 animals) underwent left coronary artery ligation. Animals were divided into 4 groups. Group 1 was injected with hpMSCs in the peri-infarct region. Groups 2 and 3 received hbmMSCs and In Vitro differentiated hbmMSCs into cardiomyocytes respectively. Cell free medium was injected in group 4. Echocardiography was performed at baseline, day 4, weeks 3, 6, and 9 after ligation. Myocardial tissues were harvested and studied immunohistochemically for specific muscular and cardiac markers (Actin and Troponin I) on weeks 6 and 10. Results: In Vitro differentiation into cardiomyocyte lineage was achieved with the hpMSCs. HpMSCs were detected within rat myocardium by week 6 after their implantation. These cells stained positively for Actin and Troponin I. Preliminary echocardiographic data show cardiac functional increase in group 1. Whether hpMSCs can provide a superior effect than hbmMSCs or differentiated hbmMSCs is being investigated. Conclusions: In Vitro studies indicated that the hpMSCs can be differentiated into cardiac cells. When implanted into the rat infarcted myocardium, hpMSCs survived and were able to differentiate into cardiomyocytes. These cells appeared to increase cardiac function in an induced myocardial infarction rat model. With the advantages of easy availability and young age, hpMSCs could be more suitable for myocardial regenerative therapy.

scholarly journals The Intrapericardial Delivery of Extracellular Vesicles from Cardiosphere-Derived Cells Stimulates M2 Polarization during the Acute Phase of Porcine Myocardial Infarction

2019 ◽  
Vol 16 (3) ◽  
pp. 612-625 ◽  
Author(s):  
Esther López ◽  
Rebeca Blázquez ◽  
Federica Marinaro ◽  
Verónica Álvarez ◽  
Virginia Blanco ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Extracellular Vesicles ◽  
Acute Phase ◽  
Peripheral Blood ◽  
Cardiac Tissue ◽  
Troponin I ◽  
Pathological Condition ◽  
Experimental Conditions ◽  
Inflammatory Phase ◽  
Arginase 1

AbstractAcute myocardial infarction triggers a strong inflammatory response in the affected cardiac tissue. New therapeutic tools based on stem cell therapy may modulate the unbalanced inflammation in the damaged cardiac tissue, contributing to the resolution of this pathological condition. The main goal of this study was to analyze the immunomodulatory effects of cardiosphere-derived cells (CDCs) and their extracellular vesicles (EV-CDCs), delivered by intrapericardial administration in a clinically relevant animal model, during the initial pro-inflammatory phase of an induced myocardial infarction. This effect was assessed in peripheral blood and pericardial fluid leukocytes from infarcted animals. Additionally, cardiac functional parameters, troponin I, hematological and biochemical components were also analyzed to characterize myocardial infarction-induced changes, as well as the safety aspects of these procedures. Our preclinical study demonstrated a successful myocardial infarction induction in all animals, without any reported adverse effect related to the intrapericardial administration of CDCs or EV-CDCs. Significant changes were observed in biochemical and immunological parameters after myocardial infarction. The analysis of peripheral blood leukocytes revealed an increase of M2 monocytes in the EV-CDCs group, while no differences were reported in other lymphocyte subsets. Moreover, arginase-1 (M2-differentiation marker) was significantly increased in pericardial fluids 24 h after EV-CDCs administration. In summary, we demonstrate that, in our experimental conditions, intrapericardially administered EV-CDCs have an immunomodulatory effect on monocyte polarization, showing a beneficial effect for counteracting an unbalanced inflammatory reaction in the acute phase of myocardial infarction. These M2 monocytes have been defined as “pro-regenerative cells” with a pro-angiogenic and anti-inflammatory activity.

scholarly journals Diagnostic Application of Postmortem Cardiac Troponin I Pericardial Fluid/Serum Ratio in Sudden Cardiac Death

Diagnostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 614
Author(s):  
Diana Hernández-Romero ◽  
María del Rocío Valverde-Vázquez ◽  
Juan Pedro Hernández del Rincón ◽  
José A. Noguera-Velasco ◽  
María D. Pérez-Cárceles ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Cardiac Troponin ◽  
Cardiac Death ◽  
Troponin I ◽  
Sampling Site ◽  
Pericardial Fluid ◽  
Cardiac Troponin I ◽  
Control Group ◽  
Complementary Method

In approximately 5% of unexpected deaths, establishing a conclusive diagnosis exclusively on the basis of anatomo-pathological findings in a classic autopsy is difficult. Postmortem biomarkers have been actively investigated as complementary indicators to help to reach valid conclusions about the circumstances of death. Several studies propose either the pericardial fluid or peripheral veins as a location for troponin determination, but the optimum sampling site is still a matter of debate. Our objective was to evaluate the association between the ratio of troponin values in the pericardial fluid and serum (determined postmortem) and the diagnosis of acute myocardial infarction (AMI) in the context of sudden cardiac death. We included 175 forensic cases. Two groups were established: AMI deaths (48; 27.4%) and the control group (127; 72.6%). The cardiac Troponin I (cTnI) values in the pericardial fluid and the troponin ratio were found to be associated with the cause of death. Univariate regression analyses showed that both age and the cTnI ratio were significantly associated with the diagnosis of AMI death. In a multivariate analysis, adjusting for confounding factors, the age and cTnI ratio were independent predictors of death from myocardial infarction. We performed a receiver operating characteristic (ROC) curve for the cTnI ratio for AMI death and selected a cut-off point. Our biomarker was found to be a valuable and highly effective tool for use in the forensic field as a complementary method to facilitate diagnosis in nonconclusive autopsies.

scholarly journals EXTH-70. ENHANCEMENT OF ANTITUMOR ACTIVITY BY USING 5-ALA–MEDIATED SONODYNAMIC THERAPY TO INDUCE APOPTOSIS AND NECROSIS IN A MOUSE GLIOMA MODEL

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi97-vi97
Author(s):  
Satoshi Suehiro ◽  
Takanori Ohnishi ◽  
Akihiro Inoue ◽  
Daisuke Yamashita ◽  
Masahiro Nishikawa ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Malignant Gliomas ◽  
Glioma Cells ◽  
High Intensity Focused Ultrasound ◽  
Control Group ◽  
Normal Brain ◽  
Sonodynamic Therapy ◽  
Cytotoxic Effects

Abstract OBJECTIVE High invasiveness of malignant gliomas frequently causes local tumor recurrence. To control such recurrence, novel therapies targeted toward infiltrating glioma cells are required. Here, we examined cytotoxic effects of sonodynamic therapy (SDT) combined with a sonosensitizer, 5-aminolevulinic acid (5-ALA), on malignant gliomas both in vitro and in vivo. METHODS In vitro cytotoxicity of 5-ALA-SDT was evaluated in U87 and U251 glioma cells and in U251Oct-3/4 glioma stemlike cells. Treatment-related apoptosis was analyzed using flow cytometry. Intracellular reactive oxygen species (ROS) were measured and the role of ROS in treatment-related cytotoxicity was examined. Effects of 5-ALA-SDT with high-intensity focused ultrasound (HIFU) on tumor growth, survival of glioma-transplanted mice, and histological features of the mouse brains were investigated. RESULTS The 5-ALA-SDT inhibited cell growth and changed cell morphology. Flow cytometric analysis indicated that 5-ALA-SDT induced apoptotic cell death. The 5-ALA-SDT generated higher ROS than in the control group, and inhibition of ROS generation completely eliminated the cytotoxic effects of 5-ALA-SDT. In the in vivo study, 5-ALA-SDT with HIFU greatly prolonged survival of the tumor-bearing mice compared with that of the control group (p < 0.05). Histologically, 5-ALA-SDT produced mainly necrosis of the tumor tissue in the focus area and induced apoptosis of the tumor cells in the perifocus area around the target of the HIFU-irradiated field. Normal brain tissues around the ultrasonic irradiation field of HIFU remained intact. CONCLUSIONS The 5-ALA-SDT was cytotoxic toward malignant gliomas. Generation of ROS by the SDT was thought to promote apoptosis of glioma cells. The 5-ALA-SDT with HIFU induced tumor necrosis in the focus area and apoptosis in the perifocus area of the HIFU-irradiated field. These results suggest that 5-ALA-SDT with HIFU may present a less invasive and tumor-specific therapy, not only for a tumor mass but also for infiltrating tumor cells in malignant gliomas.

Evaluation of Factors Associated With Elevated Levels of Platelet-Derived Microparticles in the Acute Phase of Cerebral Infarction

2009 ◽  
Vol 16 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Nagato Kuriyama ◽  
Yoshinari Nagakane ◽  
Akiko Hosomi ◽  
Tomoyuki Ohara ◽  
Takashi Kasai ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Acute Phase ◽  
Control Level ◽  
Intima Media Thickness ◽  
Vascular Lesions ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Large Artery ◽  
Vessel Occlusion ◽  
Atherosclerotic Lesions

Background: Platelet-derived microparticles (PDMPs) have attracted attention as blood coagulation-promoting, endothelial cell-activating factors. The objective of this study was to determine the parameters associated with elevated PDMP levels and examine their relationship with atherosclerotic lesions of main intracranial and extracranial arteries. Participants and Methods: Participants included a control group (C) of 61 patients with no apparent cerebral vascular lesions and 110 patients with acute-phase cerebral infarction, consisting of a small-vessel occlusion group (S) of 34 patients, a large-artery atherosclerosis group (L) of 41 patients, a cardioembolism group (CE) of 20 patients, and a stroke of undetermined etiology group (U) of 15 patients. Platelet-derived microparticle levels were measured using enzyme-linked immunosorbent assay (ELISA) at the time of admission, and the patients were reclassified into group CP (control level PDMPs), consisting of 70 patients with control PDMP levels, and group HP (high PDMPs), consisting of 40 patients with elevated PDMP levels. All patients underwent cranial magnetic resonance (MR) and carotid ultrasound examinations. Results: Platelet-derived microparticle levels were significantly higher in groups S and L than in group C (P < .01). Concomitant intima-media thickness (IMT; odds ratio [OR] = 1.29, P < .05) and concomitant intracranial stenosis (OR = 3.95, P < .01) were significantly correlated with elevated PDMP levels. Fibrinogen and high-sensitivity CRP levels were significantly higher in group HP than in group CP. Conclusion: Alterations in PDMP levels correlated with the presence of atherothrombotic lesions, and PDMP levels are expected to be useful as a clinical indicator, reflecting the presence of intracranial atherosclerotic lesions in the acute phase of cerebral infarction.

Age-associated features of the expression level of apoptosis markers in cardiomyocytes of patients with dilated cardiomyopathy

2022 ◽  
pp. 885-890
Author(s):  
К.П. Кравченко ◽  
К. Л. Козлов ◽  
А.О. Дробинцева ◽  
Д.С. Медведев ◽  
В.О. Полякова
Keyword(s):  
Cell Death ◽  
Dilated Cardiomyopathy ◽  
Molecular Mechanisms ◽  
Molecular Level ◽  
Confocal Laser ◽  
Control Group ◽  
Cellular Mechanisms ◽  
Apoptosis Pathway ◽  
Bax Protein

Для понимания патогенеза дилатационной кардиомиопатии (ДКМП) необходимо установить молекулярно-клеточные механизмы старения миокарда, в том числе связанные с программируемой клеточной гибелью, молекулярные механизмы которого практически не изучены. Цель работы - изучение маркеров апоптоза в кардиомиоцитах у пациентов с ДКМП in vitro. В работе использовали метод первичных диссоциированных клеточных культур и метод иммунофлюоресцентной конфокальной лазерной микроскопии. Для моделирования клеточного старения использовали клетки 3-го и 14-го пассажей, соответствующие «молодым» и «старым» культурам. На молекулярном уровне старение клеток кардиомиоцитов сопровождалось повышением экспрессии р16 в 2 раза по сравнению с «молодыми культурами» как в контрольной, так и в группе с ДКМП. Также установлено, что экспрессия р16 в культурах, взятых от пациентов с патологией, была в 2 раза выше, чем в аналогичных культурах от здоровых пациентов. Экспрессия р21 была повышена в группе с ДКМП по сравнению с контрольной группой, однако при старении культуры экспрессия p21 не изменялась, оставаясь на высоком уровне. Наиболее значимые различия были получены при сравнении экспрессии Bax в культуре клеток кардиомиоцитов из группы с ДКМП в «молодой» культуре с нормой - в 3,2 раза. Старение клеток миокарда на молекулярном уровне проявлялось в повышении экспрессии белка Baх, именно он является запускающим механизмом митохондриального пути апоптоза. Возможно, этот путь клеточной гибели является превалирующем при ДКМП. To understand the pathogenesis of dilated cardiomyopathy (DCMP), it is necessary to establish the molecular-cellular mechanisms of myocardial aging, including those associated with programmed cell death, the molecular mechanisms of which have not been practically studied. The aim of this work is to study markers of apoptosis in cardiomyocytes of patients with DCMP in vitro. We used the method of primary dissociated cell cultures and the method of immunofluorescence confocal laser microscopy. Cells of the 3 and 14 passages, corresponding to «young» and «old» cultures, were used to simulate cellular senescence. Results. At the molecular level, aging of cardiomyocyte cells was accompanied by a twofold increase in the expression of p16 compared to «young cultures» both in the control group and in the group with DCMP. It was also found that the expression of p16 in cultures taken from patients with pathology was 2 times higher than in similar cultures from healthy patients. The expression of p21 was increased in the group with DCMP compared to the control; however, with aging of the culture, the expression of p21 did not change, remaining at a significant level. The most significant differences were obtained when comparing the expression of Bax in the cell culture of cardiomyocytes from the group with DCMP in a «young» culture compared with the norm, 3,2 times. Aging of myocardial cells at the molecular level was manifested in an increase in the expression of the Bax protein, which is the triggering mechanism of the mitochondrial apoptosis pathway. It is possible that this pathway of cell death is prevalent in DCMP.

Abstract 177: Ticagrelor, but not Clopidogrel, Protects the Heart Against Reperfusion Injury and Improves Remodeling After Myocardial Infarction

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yumei Ye ◽  
Jose R Perez-Polo ◽  
Manjyot K Nanhwan ◽  
Sven Nylander ◽  
Yochai Birnbaum
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Reperfusion Injury ◽  
Heart Function ◽  
Oral Treatment ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Ventricular Ejection Fraction

Background: Clopidogrel (C) and Ticagrelor (T) are P2Y12 ADP receptor antagonists. In addition, ticagrelor inhibits adenosine cell uptake. In PLATO trial T reduced the incidence of the primary composite endpoint myocardial infarction, stroke or cardiovascular death over C in patients with acute coronary syndromes. Previous data show that 7d pretreatment with T limits infarct size (IS) in rats. We compared the effects of C and T, administered just before reperfusion on IS. We also assessed the effect of T and C, administered just before reperfusion and/or 6w oral treatment on cardiac remodeling. Methods: Rats underwent 30min coronary artery ligation. 1) At 25min of ischemia rats received intraperitoneal (IP) vehicle, T (10 or 30mg/kg), or C (12.5mg/kg). Area at risk (AR) was assessed by blue dye and IS by TTC staining 24h after reperfusion. 2) Rats received vehicle without (sham) or with (control) coronary ischemia, T (30mg/kg) IP (TIP), T (300mg/kg/d) oral for 6w, started a day after reperfusion (TPO), TIP+PO (TIPPO), or C (12.5mg/kg IP +62.5mg/kg/d PO for 6w). LV dimensions and function was assessed by echo at 6w. Results: 1) AR was comparable among groups. IS was 45.3±1.7% of the AR in the control group. T10 (31.5±1.8%; p=0.001) and T30 (21.4±2.6% p<0.001) significantly reduced IS, whereas C (42.4±2.6%) had no effect. Platelet aggregation in the controls was 64.7±1.3% and was comparable in T30 (24.9±1.8%) and C (23.2±1.8%) at 2h post reperfusion. T30 increased Akt, eNOS and ER1/2 phosphorylation 4h after reperfusion, whereas C had no effect. 2) Platelet aggregation at 1w oral treatment was 59.7±3.2% in the control group and was comparable in TIPPO (18.1±1.3%) and C (17.4±0.7%). Left ventricular ejection fraction was 77.6±0.9%*, 44.8±3.5%, 69.5±1.6%*, 69.2±1.0%*, 76.3±1.2%*, and 37.4±3.7% in the sham, vehicle, TIP, TPO, TIPPO and C treated group, respectively (*p<0.001 vs. vehicle). Left ventricular diameters at diastole and systole showed the same pattern. Conclusions: T, but not C, administered just before reperfusion protects against reperfusion injury. Oral T (in combination or not with acute treatment just before reperfusion) treatment for 6w improves heart function. C, despite achieving similar degree of platelet inhibition had no effect on remodeling.

In Vivo Interactions with (Tissue Culture Pretreated) Dermal Sheep Collagen

1991 ◽  
Vol 252 ◽  
Author(s):  
P. B. van Wachem ◽  
P. B. van Wachem ◽  
L. H. H. Olde Damink ◽  
P. J. Dijkstra ◽  
J. Feijen ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Cell Death ◽  
Marked Reduction ◽  
Giant Cells ◽  
In Vitro Cytotoxicity ◽  
Cell Infiltration ◽  
Cytotoxic Effects ◽  
Lipid Formation

ABSTRACTPretreatment in tissue culture (TC) was previously found to markedly reduce the in vitro cytotoxicity of two types of crosslinked dermal sheep collagens (DSC's). This in vivo study confirms our in vitro results, in that TC-pretreatment of crosslinked DSC's resulted in the marked reduction or elimination of cytotoxic effects, such as increased cell infiltration, a deviant neutrophil-morphology, lipid formation and cell death. TC-pretreatment affected the crosslinked state of both DSC's in a different way, which could be deduced from the differences in gelatin-formation and presence of giant cells from macrophage- or fibroblast-origin. The results are explained in view of the differences in crosslinking.

scholarly journals Cytokine status in patients with myocardial infarction as a possible predictor of coronary atherosclerosis severity

2020 ◽  
Vol 19 (3) ◽  
pp. 2316
Author(s):  
O. V. Khlynova ◽  
E. A. Shishkina ◽  
N. I. Abgaryan
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Atherosclerosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Coronary Artery Atherosclerosis ◽  
Tnf Α ◽  
Atherosclerosis Severity

Aim. To study the association of cytokine status with coronary atherosclerosis severity in patients with myocardial infarction (MI).Material and methods. Between 11.2018 and 07.2019, 92 patients hospitalized with MI in Perm Clinical Cardiology Dispensary were included in the study. The control group consisted of 23 patients with stable coronary artery disease. In addition to the standard examination, enzyme-linked immunosorbent assay was used to determine the levels of interleukins (IL)-6, -10, tumor necrosis factor alpha (TNF-α), C-reactive protein.Results. Significant increase in plasma IL-6, TNF-α and C-reactive protein levels in MI patients compared with the control group. The increase in the concentration of IL-6, TNF-α, as well as the IL-6/IL-10 ratio occurs in proportion to coronary atherosclerosis severity. A direct correlation of Gensini score with IL-6, TNF-α, and IL-6/IL-10 ratio was established.Conclusion. Further study of cytokine profile parameters in MI patients will help a clearer understanding pathogenesis of coronary artery atherosclerosis. An increase in concentrations of IL-6, TNF-α, and IL-6/IL-10 ratio is associated with an increase in coronary atherosclerosis severity and can be used in practice for its prediction.

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