Mechanistic Insights into Arterial Repair with Mesenchymal Stromal Cells

Psaltis, Peter J.

doi:10.1007/s10557-011-6362-0

Cited by 3 publications

(4 citation statements)

References 26 publications

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“…Despite these similar findings, Somers et al 24. observed a concurrent decrease in cytosolic STAT-3 activation, which was not seen in the present study.…”

Section: Cellular Localisation Of Stat-3 Activationcontrasting

confidence: 95%

“…The dual site activation of STAT-3 is in agreement with the findings of Somers et al .,24 who found that S1P-induced postconditioning caused an increase in STAT-3 activation in the nucleus and mitochondrion. Despite these similar findings, Somers et al 24.…”

Section: Cellular Localisation Of Stat-3 Activationsupporting

confidence: 92%

“…It was also demonstrated that STAT-3 mediates S1P-induced protection against doxorubicin-induced toxicity in isolated ventricular cardiomyocytes 23. Similarly, pharmacological postconditioning with S1P protects isolated mouse hearts against a global ischaemia–reperfusion insult via STAT-3 activation in the mitochondrion and nucleus,24 therefore suggesting a link between S1P and STAT-3, and hence activation of the SAFE pathway by S1P. However whether the same mechanism of protection is involved in S1P-induced preconditioning remains unknown.…”

Section: Introductionmentioning

confidence: 96%

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Cardiac preconditioning with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3 : cardiovascular topic

Kelly-Laubscher¹,

King²,

Hacking³

et al. 2014

CVJA

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SummaryAimsSphingosine-1-phosphate (S1P) is a cardioprotective agent. Signal transducer and activator of transcription 3 (STAT-3) is a key mediator of many cardioprotective agents. We aimed to explore whether STAT-3 is a key mediator in S1P-induced preconditioning.MethodsLangendorff-perfused hearts from Wistar rats and wild-type or cardiomyocyte-specific STAT-3 knockout mice were pre-treated with S1P (10 nmol/l), with or without the STAT-3 pathway inhibitor AG490, before an ischaemia–reperfusion insult. Triphenyltetrazolium chloride and Evans blue staining were used for the determination of infarct size. Western blot analysis was carried out on the S1P pre-treated hearts for detection of cytosolic, nuclear and mitochondrial phosphorylated and total STAT-3 proteins.ResultsPre-treatment with S1P decreased the infarct size in isolated rat (5 ± 3% vs control 26 ± 8%, p < 0.01) and wild-type mouse hearts (13 ± 1% vs control 33 ± 3%, p < 0.05). This protective effect was abolished in the rat hearts pre-treated with AG490 (30 ± 10%, p = ns vs control) and in the hearts from STAT-3 knockout mice (35 ± 4% vs control 30 ± 3%, p = ns). Levels of phosphorylated STAT-3 were significantly increased in both the nuclear (p < 0.05 vs control) and mitochondrial (p < 0.05 vs control) fractions in the S1P pre-treated hearts, but remained unchanged in the cytosolic fraction (p = ns vs control).ConclusionThese novel results demonstrate that pharmacological preconditioning with S1P in the isolated heart is mediated by activation of mitochondrial and nuclear STAT-3, therefore suggesting that S1P may be a novel therapeutic target to modulate mitochondrial and nuclear function in cardiovascular disease in order to protect the heart against ischaemia–reperfusion.

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“…Despite these similar findings, Somers et al 24. observed a concurrent decrease in cytosolic STAT-3 activation, which was not seen in the present study.…”

Section: Cellular Localisation Of Stat-3 Activationcontrasting

confidence: 95%

Section: Cellular Localisation Of Stat-3 Activationsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Cardiac preconditioning with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3 : cardiovascular topic

Kelly-Laubscher¹,

King²,

Hacking³

et al. 2014

CVJA

View full text Add to dashboard Cite

show abstract

“…The inflammatory cytokines, tumor necrosis factor (TNF)-α, and IL-6 released at the injury site mobilized endogenous bone-marrow-derived cells which played an important role in the process of neointimal hyperplasia after vascular injury [62]. Another important early target for the paracrine influence of exogenous MSC transfer are the resident stem cells [63]. Pericyte-like cells or MSCs from the adventitia are reported to contribute to restenosis, and these cells are found to be higher in injured arteries [64].…”

Section: Vascular Repair By Msc Paracrine Factors In Restenosismentioning

confidence: 99%

Mesenchymal Stem Cell Paracrine Factors in Vascular Repair and Regeneration

Pankajakshan¹,

Agrawal²

2014

J Biomed Tech Res

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Mesenchymal stem cell therapy show great optimism in the treatment of several diseases. MSCs are attractive candidates for cell therapy because of easy isolation, high expansion potential giving unlimited pool of transplantable cells, low immunogenicity, amenability to ex vivo genetic modification, and multipotency. The stem cells orchestrate the repair process by various mechanisms such as transdifferentiation, cell fusion, microvesicles or exosomes and most importantly by secreting paracrine factors. The MSCs release several angiogenic, mitogenic, anti-apoptotic, anti-inflammatory and anti-oxidative factors that play fundamental role in regulating tissue repair in various vascular and cardiac diseases. The therapeutic release of these factors by the cells can be enhanced by several strategies like genetic modification, physiological and pharmacological preconditioning, improved cell culture and selection methods, and biomaterial based approaches. The current review describes the impact of paracrine factors released by MSCs on vascular repair and regeneration in myocardial infarction, restenosis and peripheral artery disease, and the various strategies adopted to enhance the release of these paracrine factors to enhance organ function.

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HUCMNCs protect vascular endothelium and prevent ISR after endovascular interventional therapy for vascular diseases in T2DM rabbits

Ding

Zhang²,

et al. 2017

Mol Cell Biochem

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The therapeutic effect of transplantation of human umbilical cord blood cell-derived mononuclear cells (HUCMNCs) on treating in-stent restenosis (ISR) after endovascular interventional therapy (EIT) was evaluated in preclinical rabbit model of type 2 diabetes mellitus (T2DM)-related peripheral artery disease (PAD). HUCMNCs were transplanted to T2DM rabbits subjected to femoral artery occlusion surgery and received EIT. Serum concentration of soluble vascular endothelial cadherin (VE-cad) and plasma concentration of lipoprotein-associated phospholipase A2 (Lp-PLA2) were determined with enzyme-linked immunosorbent assay before and after the transplantation. The injury and the recovery of right femoral artery at stenting site were evaluated with Hematoxylin and Eosin (HE) staining. HUCMNCs purified from umbilical cord blood were 100% CD45 and 96.5% CD34 with round or oval morphology and adherent growth pattern. The soluble VE-cad and Lp-PLA2 were significantly attenuated after HUCMNC transplantation. The intimal area and the ratio between intimal area and medium film area in the dilated occlusion site were also dramatically decreased 4 weeks after receiving HUCMNCs. HUCMNC transplantation is effective in protecting vascular endothelial function and preventing ISR after EIT in T2DM rabbits suffering from PAD.

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Mechanistic Insights into Arterial Repair with Mesenchymal Stromal Cells

Cited by 3 publications

References 26 publications

Cardiac preconditioning with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3 : cardiovascular topic

Cardiac preconditioning with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3 : cardiovascular topic

Mesenchymal Stem Cell Paracrine Factors in Vascular Repair and Regeneration

HUCMNCs protect vascular endothelium and prevent ISR after endovascular interventional therapy for vascular diseases in T2DM rabbits

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