Abstract 36: Cardiac Progenitor Cell Lineage Tracing During Embryonic Cardiomyogenesis

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Bingyan J Wang ◽  
Alvin Muliono ◽  
Roberto Alvarez ◽  
Mark A Sussman
Keyword(s):  
Adoptive Transfer ◽  
Connexin 43 ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Lineage Tracing ◽  
Left Ventricular Myocardium ◽  
Post Injection ◽  
Term Survival

Introduction: Stem cell therapy represents great promises to myocardium regeneration. Multipotent c-Kit pos cardiac progenitor cells (CPCs) are able to differentiate into endothelial cells, smooth muscle cells, and cardiomyocytes. However, fundamental knowledge of CPC biology remains incomplete. Studies in rodent myocardial infarction model revealed that CPCs have poor long-term survival and engraftment after adoptive transfer, perhaps due to the severely damaged host environment. Therefore, it is critical to understand how CPCs interface with the recipient environment following transfer in order to enhance their true regenerative potentials. Hypothesis: Adoptively transferred stem cells are thought to survive and engraft best in an environment closely resembling their original habitat. Thus, we hypothesized that the embryonic environment provides the optimal spatiotemporal conditions to promote CPCs engraftment and commitment to cardiac fate. Methods: CPCs isolated from adult mouse hearts were expanded, fluorescence-tagged, and injected into blastocysts at E3.75 and in utero at E15.5. Embryos were analyzed following cardiogenesis by immunofluorescence for presence of CPC-derived tissues. Additionally, CPCs were injected intramyocardially at various stages from P0 to P7, to follow long-term adoptive transfer and assess CPCs lineage commitment. Results and Conclusions: At 48 hours post injection, donor CPCs were found anchoring in blastocoel and trophoblasts at E5.5, and were detected within the host myocardium at E17.5 predominantly at perivascular regions (n=4). Interestingly, CPCs also integrated into aminochorionic sac, indicating a novel non-cardiogenic fate of CPCs (n=5). CPCs injected at P3 stably engrafted into left ventricular myocardium by 14 days post injection (n=4), sharing gap junction proteins (ZO-1, Connexin-43) with neighboring cells. In conclusion, this study provides vivid evidence for the first time of CPC engraftment and survival in vivo under homeostasis during cardiogenesis. Future studies will assess the permissive environmental conditions, which may optimize their use in therapeutic applications, and the cardiogenic potential of CPCs in order to provide fundamental insights on CPCs biology.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

scholarly journals Case Report: A Giant Left-Ventricular Intramural Pseudoaneurysm Arise From Ruptured Left Sinus of Valsalva Aneurysm

2021 ◽  
Vol 8 ◽  
Author(s):  
Minghui Hua ◽  
Yufan Gao ◽  
Jianhui Li ◽  
Fang Tong ◽  
Ximing Li ◽  
...  
Keyword(s):  
Imaging Techniques ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Patch Repair ◽  
Left Ventricular Myocardium ◽  
Sinus Of Valsalva Aneurysm ◽  
Sinus Valsalva Aneurysm ◽  
Left Sinus Of Valsalva

In this report, we present a case study of an extremely rare left sinus Valsalva aneurysm (SVA) rupture into the left-ventricular myocardium. Acute ozone inhalation and long-term hypertension are possible contributors to the condition. Utilizing multimodal cardiovascular imaging techniques [echocardiogram, computed tomography (CT), and cardiac magnetic resonance (CMR)], a large, left-ventricular, intramural pseudoaneurysm (IPA) arising from the ruptured left SVA, was clearly observed anatomically and functionally. Subsequently, our patient underwent patch repair and valvoplasty which offered an excellent prognosis. This report describes the manifestation of the ruptured left SVA and its possible etiology. This case also emphasizes the need for multimodal imaging for subsequent surgical repair.

Immuno-Enzyme Histochemistry of Creatine Phosphokinase

1977 ◽  
Vol 35 ◽  
pp. 446-447
Author(s):  
N. Baba ◽  
E.T. Poe ◽  
J. Scillian ◽  
T. Myser
Keyword(s):  
Creatine Phosphokinase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Rabbit Muscle ◽  
Cytoplasmic Staining ◽  
Heart Muscle Cells ◽  
Diffuse Cytoplasmic Staining ◽  
Strong Staining

With a commercially available rabbit muscle (MM) type isoenzyme of the creatine phosphokinase (CPK) (Worthington Biochemical), anti-CPK antibody was produced in chicken and goat (Figure 1). Fab' fragments of the chicken and goat IgG were isolated and conjugated with a commercially available horseradish peroxidase (HRP) according to the Nakane method (J. Histochem. Cytochem,, 22:1084, 1974).Rabbit hearts were perfused in vivo with freshly prepared 2% paraformaldehyde solution, and the left ventricular myocardium was fixed for 30 minutes. Forty-micrometer-thick frozen sections of the myocardium were incubated with the Fab'-HRP conjugate overnight at 4°C. After a thorough rinse, the sections were stained for the peroxidase reaction.In an electron microscope, diffuse cytoplasmic staining of the heart muscle cells was noted, indicating the diffuse cytosol distribution of CPK (Figure 2). In addition, there was strong staining of the intermembranous and intracristal space of the mitochondria as well as the M-lines of the myofibrils (Figures 3 and 4).

In vivo detection of endogenous acetylcholine release in cat ventricles

1994 ◽  
Vol 266 (3) ◽  
pp. H854-H860 ◽  
Author(s):  
T. Akiyama ◽  
T. Yamazaki ◽  
I. Ninomiya
Keyword(s):  
Nerve Stimulation ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Left Ventricular Myocardium ◽  
Ach Release ◽  
Vagal Nerves ◽  
Dialysis Technique

To detect and monitor endogenous acetylcholine (ACh) release in the in vivo heart, we applied a dialysis technique to the hearts of anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and were perfused with Krebs-Henseleit solution containing Eserine (10(-4) M) at 3 microliters/min. Dialysate ACh concentration was measured with high-performance liquid chromatography. In four cats, the response to vagal stimulation was studied. Electrical stimulation of efferent vagal nerves (10 Hz) significantly increased dialysate ACh concentration from 596 +/- 118 (control) to 12,210 +/- 1,661 pM. After stimulation, dialysate ACh concentration significantly decreased to 382 +/- 80 pM below control. The influence of ganglionic blocker was determined in six cats. Control vagal nerve stimulation (10 Hz) increased dialysate ACh concentration from 582 +/- 136 to 9,102 +/- 754 pM. Local perfusion of hexamethonium (10(-4) M) did not affect this nerve stimulation-induced ACh increase (8,611 +/- 1,189 pM), and intravenous administration of hexamethonium (20 mg/kg) prevented this increase (340 +/- 88 pM). We examined the response to vagal nerve stimulation at different frequencies in three cats. Vagal nerve stimulation increased dialysate ACh concentration from a control of 588 +/- 211 to 1,227 +/- 195 pM at 2 Hz, 3,946 +/- 1,059 pM at 5 Hz, and 9,366 +/- 1,873 pM at 10 Hz. Dialysate ACh concentration reflects ACh release from postganglionic vagal nerves innervating the left ventricular myocardium; the dialysis technique permits estimation of relative changes in efferent cardiac vagal nerve activity.

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