Injured cardiomyocytes promote dental pulp mesenchymal stem cell homing

Scipio, Federica Di; Sprio, Andrea Elio; Folino, Anna; Carere, Maria Elisabetta; Salamone, Paolina; Yang, Zhiqian; Berrone, Mattia; Prat, María; Losano, G; Rastaldo, Raffaella; Berta, Giovanni Nicolao

doi:10.1016/j.bbagen.2014.03.005

Cited by 16 publications

(14 citation statements)

References 61 publications

(104 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, we also did not perform the study to track stem cell movement. However, the previous study has shown that dental stem cells can migrate to the damaged tissue, growth factors and paracrine factors such as SDF-1, HGF and VGEF from dental pulp stem cells are the keys that involved as chemotactic and homing of stem cells to the damaged tissue/cells [27,28]. Paracrine effects are a possible mechanism that enhances neovascularization, reduces inflammation and is involved in the heart remodeling.…”

Section: Discussionmentioning

confidence: 99%

Intravenous administration of puppy deciduous teeth stem cells in degenerative valve disease

Petchdee

Sompeewong

2016

Vet World

View full text Add to dashboard Cite

Aim:The objective of this study is to investigate the improvement of heart function in dogs with chronic valvular heart disease after puppy deciduous teeth stem cells (pDSCs) administration.Materials and Methods:20 client-owned dogs with degenerative valvular heart disease underwent multiple intravenous injections of allogeneic pDSCs. Dogs were randomly assigned to two groups: (i) Control group (n=10) with standard treatment for heart failure and (ii) group with standard treatment and multiple administrations of pDSCs (n=10). Electrocardiography, complete transthoracic echocardiography, thoracic radiography, and blood pressure were recorded before and after pDSCs injections for 15, 30 and 60 days.Results:Post pDSCs injection showed measurable improvement in left ventricular ejection fraction, American College of Veterinary Internal Medicine (ACVIM) functional class significantly improved and improved quality of life scores were observed. In the control group, there were no significant enhancements in heart function or ACVIM class.Conclusions:This finding suggests that pDSCs could be a supplement for valvular heart disease treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Intravenous administration of puppy deciduous teeth stem cells in degenerative valve disease

Petchdee

Sompeewong

2016

Vet World

View full text Add to dashboard Cite

show abstract

“…42,43 Here, we show that ticagrelor, but not clopidogrel, attenuates the increase in MIP-2 4 weeks after myocardial infarction. However, FGF-2 induces cardioprotection, 44 has a role as a chemotactic factor for stem cell homing after myocardial injury, 45 induces angiogenesis, 46,47 and improves remodeling after myocardial infarction in the rat. [48][49][50] The significance of the ticagrelorinduced attenuation and clopidogrel-induced normalization of the increase in FGF-2 levels 4 weeks after infarction is unclear.…”

Section: Discussionmentioning

confidence: 99%

Ticagrelor Protects the Heart Against Reperfusion Injury and Improves Remodeling After Myocardial Infarction

Ye¹,

Birnbaum

Perez‐Polo

et al. 2015

ATVB

108

111

View full text Add to dashboard Cite

Objective-In addition to P2Y 12 receptor antagonism, ticagrelor inhibits adenosine cell uptake. Prior data show that 7-day pretreatment with ticagrelor limits infarct size. We explored the acute effects of ticagrelor and clopidogrel on infarct size and potential long-term effects on heart function. Approach and Results-Rats underwent 30-minute ischemia per 24-hour reperfusion. (1) Ticagrelor (10 or 30 mg/kg) or clopidogrel (12.5 mg/kg) was given via intraperitoneal injection 5 minutes before reperfusion. (2) Rats received ticagrelor acute (intraperitoneal; 30 mg/kg), chronic (oral; 300 mg/kg per day) for 4 weeks starting 1 day after reperfusion or the combination (acute+chronic). Another group received clopidogrel (intraperitoneal [12.5 mg/kg]+oral [62.5 mg/kg per day]) for 4 weeks.(1) Ticagrelor dose-dependently reduced infarct size, 10 mg/kg (31.5%±1.8%; P<0.001) and 30 mg/ kg (21.4%±2.6%; P<0.001) versus control (45.3±1.7%), whereas clopidogrel had no effect (42.4%±2.6%). Ticagrelor, but not clopidogrel, increased myocardial adenosine levels, increased phosphorylation of Akt, endothelial NO synthase, and extracellular-signal-regulated kinase 1/2 4 hours after reperfusion and decreased apoptosis. (2) After 4 weeks, left ventricular ejection fraction was reduced in the vehicle-treated group (44.8%±3.5%) versus sham (77.6%±0.9%).All ticagrelor treatments improved left ventricular ejection fraction, acute (69.5%±1.6%), chronic (69.2%±1.0%), and acute+chronic (76.3%±1.2%), whereas clopidogrel had no effect (37.4%±3.7%). Ticagrelor, but not clopidogrel, attenuated fibrosis and decreased collagen-III mRNA levels 4 weeks after ischemia/reperfusion. Ticagrelor, but not clopidogrel, attenuated the increase in proinflammatory tumor necrosis factor-α, interleukin-1β, and interleukin-18, and increased anti-inflammatory 15-epi-lipoxin-A 4 levels. Conclusions-Ticagrelor, but not clopidogrel, administered just before reperfusion protects against reperfusion injury. This acute treatment or chronic ticagrelor for 4 weeks or their combination improved heart function, whereas clopidogrel, despite achieving a similar degree of platelet inhibition, had no effect. addition to platelet inhibition, ticagrelor, but not clopidogrel, has protective effects against ischemia-reperfusion that may help explain the differences in clinical benefit in the PLATO trial. 7,8 However, a recent multicenter, randomized, double-blind clinical trial did not show a clear clinical benefit in patients with STEMI receiving ticagrelor en route to the hospital versus in the catheterization laboratory. 16 As the study was not powered for benefit on cardiovascular events, it is inconclusive about the hypothesis that administration of ticagrelor after onset of ischemia (in contrast to pretreatment just before reperfusion) can ameliorate reperfusion injury. In addition, as the median time difference between the prehospital and the in-hospital ticagrelor administration groups was only 31 minutes, 16 it is plausible that ticagrelor absorption was insufficient an...

show abstract

“…Two month-old male Wistar rats (Harlan-Italy, S. Pietro al Natisone, Italy) received humane care in compliance with Italian law (DL-116, January ST-segment 27,1992) …”

Section: Animalsmentioning

confidence: 99%

Alpha-linolenic acid protects against cardiac injury and remodelling induced by beta-adrenergic overstimulation

et al. 2015

Self Cite

View full text Add to dashboard Cite

We investigated the effect of α-linolenic acid (ALA) in protecting the heart from injury caused by β-adrenergic overstimulation. ALA's role either in isoproterenol (ISO)-treated isolated rat cardiomyocytes (H9c2 cells) or in in vivo rat hearts was studied. In isolated cardiomyocytes in vitro, the involvement of kinases (Src and PI3K) in protection was tested using the specific inhibitors (PP2 or LY294002 respectively), while the role of caveolae was assessed by their disruption with methyl-β-cyclodextrin. The rats underwent either a normal chow diet or, alternatively, an ALA-enriched diet before, during and throughout the 60 days after 5 days of isoproterenol administration. Before sacrifice, the hemodynamic changes were measured using echocardiography. In the explanted hearts, histological changes together with molecular markers of cardiac fibrosis and hypertrophy were evaluated. In H9c2 cells, ALA abolished the ISO-induced reduction of viability. This effect was suppressed by both the inhibitor PP2 or LY294002 and the caveolae disrupter methyl-β-cyclodextrin. In the rats, ALA prevented ISO-induced myocardial fibrosis and hypertrophy and kept the cardiac mechanical function as in the control. It also counteracted the increased expressions of transforming growth factor-β (TGF-β) and β-myosin (β-MHC), the decreased expression of tissue inhibitor metalloproteinase-1 (TIMP-1) and the enhanced activity of matrix metalloproteinase-2 (MMP-2). In conclusion, ALA-induced protection requires the integrity of caveolae where β2-adrenergic receptors (β2ARs) are restricted and mediate the activation of the Src-PI3K protective pathway. By preserving this β2AR pro-survival pathway, an ALA-enriched diet protects the heart against ISO-induced fibrosis and hypertrophy.

show abstract

Injured cardiomyocytes promote dental pulp mesenchymal stem cell homing

Cited by 16 publications

References 61 publications

Intravenous administration of puppy deciduous teeth stem cells in degenerative valve disease

Intravenous administration of puppy deciduous teeth stem cells in degenerative valve disease

Ticagrelor Protects the Heart Against Reperfusion Injury and Improves Remodeling After Myocardial Infarction

Alpha-linolenic acid protects against cardiac injury and remodelling induced by beta-adrenergic overstimulation

Contact Info

Product

Resources

About