Cardiomyocyte apoptosis in ischaemia‐reperfusion due to the exogenous oxidants at the time of reperfusion

Rosca, Ana‐Maria; Matei, Camelia; Dragan, Emanuel; Burlacu, Alexandrina

doi:10.1042/cbi20120080

Cited by 9 publications

(6 citation statements)

References 33 publications

(43 reference statements)

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“…We now provided evidence that 25-OHC injection resulted in reduced levels of p-Bad and increased levels of cleaved caspase-3 in mouse gastrocnemius muscles. In addition to activation of Bad, 25-OHC has also been shown to induce apoptosis in cardiomyocytes, smooth muscle cells, and PC-12 cells via the production of reactive oxygen species and activation of GSK3β (Appukuttan et al, 2013, Choi et al, 2008, Lee da et al, 2015, Rosca et al, 2012, Sekiya et al, 2014). …”

Section: Discussionmentioning

confidence: 99%

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

et al. 2017

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While angiotensin II (ang II) has been implicated in the pathogenesis of cardiac cachexia (CC), the molecules that mediate ang II's wasting effect have not been identified. It is known TNF-α level is increased in patients with CC, and TNF-α release is triggered by ang II. We therefore hypothesized that ang II induced muscle wasting is mediated by TNF-α. Ang II infusion led to skeletal muscle wasting in wild type (WT) but not in TNF alpha type 1 receptor knockout (TNFR1KO) mice, suggesting that ang II induced muscle loss is mediated by TNF-α through its type 1 receptor. Microarray analysis identified cholesterol 25-hydroxylase (Ch25h) as the down stream target of TNF-α. Intraperitoneal injection of 25-hydroxycholesterol (25-OHC), the product of Ch25h, resulted in muscle loss in C57BL/6 mice, accompanied by increased expression of atrogin-1, MuRF1 and suppression of IGF-1/Akt signaling pathway. The identification of 25-OHC as an inducer of muscle wasting has implications for the development of specific treatment strategies in preventing muscle loss.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

et al. 2017

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“…The results of the present study suggest that the role of NRG-1 in cardiac protection is conferred through activation of the Akt pathway, which is associated with an increase in the level of bcl-2 expression and reduction in the level of bax expression. The ratio of bax/bcl-2 is known to be an important marker of cardiomyocyte apoptosis (31,32). …”

Section: Discussionmentioning

confidence: 99%

Gene transfer of human neuregulin-1 attenuates ventricular remodeling in diabetic cardiomyopathy rats

Xiao

et al. 2013

Experimental and Therapeutic Medicine

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Neuregulin-1 (NRG-1) is a cardioactive growth factor released from endothelial cells. However, the effect of NRG-1 on ventricular remodeling in diabetic cardiomyopathy (DCM) remains unclear. The aim of the present study was to investigate the pathophysiological role of NRG-1 in a rat model of DCM. Rat cardiac microvascular endothelial cells (CMECs) were transfected with human NRG-1 (hNRG-1) lentivirus. The hNRG-1 medium was utilized to culture rat cardiomyocytes. The cardiomyocytes were counted with a hemacytometer to determine the proliferation index and Annexin V/propidium iodide double staining was employed to examine the apoptotic rate. A rat model of DCM was induced by an intraperitoneal injection of streptozotocin. The hNRG-1 lentivirus was injected into the myocardium of the DCM model rats. Four weeks after the lentiviral injection, cardiac catheterization was performed to evaluate the cardiac function. Apoptotic cells were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. Left ventricular sections were stained with Masson’s trichrome to investigate the myocardial collagen content. The expression levels of related genes and proteins were analyzed. The results indicated that hNRG-1 conditioned medium stimulated the proliferation and counteracted the apoptosis of cardiomyocytes in vitro. In the rats with DCM, gene transfer of hNRG-1 to the myocardium improved heart function, as indicated by invasive hemodynamic measurements. In addition, hNRG-1 reduced the number of apoptotic cells, decreased the expression of bax and increased the expression of bcl-2 in the myocardium of the DCM model rats. Myocardial fibrosis and type I and III pro-collagen mRNA levels in the myocardium were significantly reduced by hNRG-1. hNRG-1 also increased the expression of phospho-Akt and phospho-eNOS in the myocardium. In conclusion, the gene transfer of hNRG-1 ameliorates cardiac dysfunction in diabetes. Although further studies are required, NRG-1 appears to protect cardiomyocytes against apoptosis and to reduce the extent of myocardial interstitial fibrosis.

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“…Valinomycin is known as a cargo that easily interacts and internalizes into cells. The effectiveness of valinomycin entrapped into Fe-PEI aggregates was assessed by evaluation of the mitochondrial membrane potential (ΔΨm) in MSCs after cell interaction with valinomycin-Fe-PEI aggregates using JC-1 [ 26 ]. As revealed in Figure 3 d, ΔΨm was almost completely lost after 24-h exposure of MSCs to valinomycin-Fe-PEI aggregates, to a similar extent to MSCs exposed to the same dose of valinomycin given as such.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of the Ability of Nanostructured PEI-Coated Iron Oxide Nanoparticles to Incorporate Cisplatin during Synthesis

Ţuţuianu¹,

Popescu

Preda³

et al. 2017

Nanomaterials

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Nanoparticles (NPs) have a high potential for biological applications as they can be used as carriers for the controlled release of bioactive factors. Here we focused on poly(ethylenimine) (PEI)-coated iron oxide hybrid NPs obtained by hydrothermal synthesis in high pressure conditions and evaluated their behavior in culture medium in the presence or absence of cells, as well as their ability to incorporate antitumor drug cisplatin. Our results showed that the hydrothermal conditions used for Fe-PEI NPs synthesis allowed the incorporation of cisplatin, which even increased its anti-tumor effects. Furthermore, the commonly occurring phenomenon of NPs aggregation in culture medium was exploited for further entrapment of other active molecules, such as the fluorescent dye DiI and valinomycin. The molecules bound to NPs during synthesis or during aggregation process were delivered inside various cells after in vitro and in vivo direct contact between cells and NPs and their biological activity was preserved, thus supporting the therapeutic value of Fe-PEI NPs as drug delivery tools.

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Cardiomyocyte apoptosis in ischaemia‐reperfusion due to the exogenous oxidants at the time of reperfusion

Cited by 9 publications

References 33 publications

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

Gene transfer of human neuregulin-1 attenuates ventricular remodeling in diabetic cardiomyopathy rats

Evaluation of the Ability of Nanostructured PEI-Coated Iron Oxide Nanoparticles to Incorporate Cisplatin during Synthesis

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