Conditioned medium of H9c2 triggers VEGF dependent angiogenesis by activation of p38/pSTAT3 pathways in placenta derived stem cells for cardiac repair

Makhoul, Georges; Jurakhan, Rishi; Jaiswal, Prashant Kumar; Ridwan, Khalid; Li, Li; Selvasandran, Kaviyanka; Duong, Minh; Schwertani, Adel; Cecere, Renzo

doi:10.1016/j.lfs.2016.04.009

Cited by 9 publications

(7 citation statements)

References 32 publications

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“…Moreover, UCB-MSCs have been shown to differentiate into functional EPCs following induction with VEGF and hFGF, and the formation of vessel-like structures has been observed following a period of growth (Sabry et al, 2016). Placenta-derived MSCs also exhibit the ability to differentiate into endothelial-like cells and smooth muscle-like cells when cultured with VEGF (Makhoul et al, 2016). Placenta-derived MSCs can also be induced so to express neural phenotypes, displaying neuronal markers, such as GFAP, Nestin, or β-Tubulin III (Martini et al 2013).…”

Section: Identifying the Optimal Cell Type For Stem Cell Transplanmentioning

confidence: 99%

Stem cell therapy for abrogating stroke-induced neuroinflammation and relevant secondary cell death mechanisms

Stonesifer

Corey

Ghanekar

et al. 2017

Progress in Neurobiology

203

207

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Ischemic stroke is a leading cause of death worldwide. A key secondary cell death mechanism mediating neurological damage following the initial episode of ischemic stroke is the upregulation of endogenous neuroinflammatory processes to levels that destroy hypoxic tissue local to the area of insult, induce apoptosis, and initiate a feedback loop of inflammatory cascades that can expand the region of damage. Stem cell therapy has emerged as an experimental treatment for stroke, and accumulating evidence supports the therapeutic efficacy of stem cells to abrogate stroke-induced inflammation. In this review, we investigate clinically relevant stem cell types, such as hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs), endothelial progenitor cells (EPCs), very small embryonic-like stem cells (VSELs), neural stem cells (NSCs), extraembryonic stem cells, adipose tissue-derived stem cells, breast milk-derived stem cells, menstrual blood-derived stem cells, dental tissue-derived stem cells, induced pluripotent stem cells (iPSCs), teratocarcinoma-derived Ntera2/D1 neuron-like cells (NT2N), c-mycER(TAM) modified NSCs (CTX0E03), and notch-transfected mesenchymal stromal cells (SB623), comparing their potential efficacy to sequester stroke-induced neuroinflammation and their feasibility as translational clinical cell sources. To this end, we highlight that MSCs, with a proven track record of safety and efficacy as a transplantable cell for hematologic diseases, stand as an attractive cell type that confers superior anti-inflammatory effects in stroke both in vitro and in vivo. That stem cells can mount a robust anti-inflammatory action against stroke complements the regenerative processes of cell replacement and neurotrophic factor secretion conventionally ascribed to cell-based therapy in neurological disorders.

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Section: Identifying the Optimal Cell Type For Stem Cell Transplanmentioning

confidence: 99%

Stem cell therapy for abrogating stroke-induced neuroinflammation and relevant secondary cell death mechanisms

Stonesifer

Corey

Ghanekar

et al. 2017

Progress in Neurobiology

203

207

View full text Add to dashboard Cite

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“…Experiments were conducted in accordance with the Canadian Council on Animal Care regulations and were approved by the McGill University Health Centre Ethics Committee. A left anterolateral thoracotomy was performed in three of the four groups (n ¼ 12) of Lewis rats (Charles River Laboratories, Quebec, Canada), and an ischemic MI was surgically induced by using a left anterior descending artery ligation procedure with a 7.0 polypropylene suture (Ethicon, Somerville, NJ) under sterile conditions [12][13][14]. The fourth group did not undergo an MI and remained as the baseline group.…”

Section: Rat MI Model and Secretome Treatmentmentioning

confidence: 99%

A Tumor Necrosis Factor-α and Hypoxia-Induced Secretome Therapy for Myocardial Repair

Selvasandran

Makhoul

Jaiswal

et al. 2018

The Annals of Thoracic Surgery

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“…These cells were incubated for 48 h. After conducting the initial procedures followed in the stains described above (media aspiration, fixation and PBS washing), DAPI staining solution (0.5

μ

g/ml in PBS) was added to each well in dark and the plate was incubated for 15 min on rocker at room temperature. Slides were mounted and observed under fluorescent microscope (Olympus Corporation) in dark using the DAPI filter (D'amico et al ., ; Makhoul et al ., ). Images were captured using ProgRes capture Pro 2.7 software.…”

Section: Methodsmentioning

confidence: 97%

Cardioprotective potential of curcumin against norepinephrine‐induced cell death: a microscopic study

Manghani

Gupta

Tripathi

et al. 2016

Journal of Microscopy

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Cardiomyopathy and associated heart failure continues to be one of the most severe complications that threaten a large population. Curcumin, one of the three curcuminoids of the spice turmeric, is very well known for a multitude of health benefits and functions. Norepinephrine (NE), a catecholamine and also a stress hormone may cause the cardiomyocytes to develop increased sensitivity to death with its increasing concentrations. In this study, we investigated the cardioprotective effect of curcumin in NE-induced cardiac apoptosis using several fluorescent and nonfluorescent microscopic techniques like DAPI, PI, Giemsa, PicroSirius and TUNEL. The aim of the study was to assess the effect of curcumin in preventing the occurrence of features underlying apoptosis such as nuclear disruption, chromatin condensation, DNA fragmentation and alterations in mitochondrial membrane permeability. Our results show that curcumin protects the cardiomyocytes against apoptosis significantly and also helps them to revert to their normal physiological state. Hence, we propose that curcumin has the potential to act as a therapeutic agent for the attenuation of NE-induced cardiac cell death and modulation of apoptosis in H9c2 cardiomyocytes.

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Conditioned medium of H9c2 triggers VEGF dependent angiogenesis by activation of p38/pSTAT3 pathways in placenta derived stem cells for cardiac repair

Cited by 9 publications

References 32 publications

Stem cell therapy for abrogating stroke-induced neuroinflammation and relevant secondary cell death mechanisms

Stem cell therapy for abrogating stroke-induced neuroinflammation and relevant secondary cell death mechanisms

A Tumor Necrosis Factor-α and Hypoxia-Induced Secretome Therapy for Myocardial Repair

Cardioprotective potential of curcumin against norepinephrine‐induced cell death: a microscopic study

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