Pretreatment With Argon Protects Human Cardiac Myocyte-Like Progenitor Cells from Oxygen Glucose Deprivation-Induced Cell Death by Activation of AKT and Differential Regulation of Mapkinases

Qi, Hong; Soto-Gonzalez, Lourdes; Krychtiuk, Konstantin A.; Ruhittel, Sarah; Kaun, Christoph; Speidl, Walter S.; Kiss, Attila; Podesser, Bruno K.; Yao, Shanglong; Markstaller, Klaus; Klein, Klaus Ulrich; Tretter, Verena

doi:10.1097/shk.0000000000000998

Cited by 13 publications

(15 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies have shown that inert gas argon pre-treatment influences OGD-induced oxidative damage of human cardiomyocytes. Qi et al reported that cardiomyocytes pre-treated with 30% argon for 90 min significantly increased cell activity and inhibited apoptosis [ 4 ]. In the present study, after pre-treatment with 50% argon for 1 h, the viability of cardiomyocytes induced by OGD increased and the apoptosis rate decreased significantly, which was similar to previous results.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, inert gas has become a research hotspot because of its potential organ protective effect. Argon, as one of the main components, has a protective effect on nerves and myocardium after ischemia reperfusion injury [3][4][5][6]. In vivo, 30% and 50% argon pre-treatment significantly reduced the apoptosis and inflammation level and improved the cell survival rate in human cardiomyocytes by AKT activation and differential regulation of MAP kinases [4].…”

Section: Introductionmentioning

confidence: 99%

“…Argon, as one of the main components, has a protective effect on nerves and myocardium after ischemia reperfusion injury [3][4][5][6]. In vivo, 30% and 50% argon pre-treatment significantly reduced the apoptosis and inflammation level and improved the cell survival rate in human cardiomyocytes by AKT activation and differential regulation of MAP kinases [4]. Kiss et al found that argon-mediated protection of myocardial tissue may be related to JNK and high-mobility group box 1 [5].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Zhang

Shang

et al. 2021

Bioengineered

Self Cite

View full text Add to dashboard Cite

The objective of this study was to explore the effect of argon preconditioning on myocardial ischemia reperfusion (MI/R) injury and its mechanism. Cardiomyocytes H2C9 were pre-treated with 50% argon, and a cell model of oxygen-glucose deprivation (OGD) was established. CCK-8 and cytotoxicity detection kits were used to detect cell viability and lactate dehydrogenase (LDH) release. The miR-21 expression was detected using quantitative real-time polymerase chain reaction. Western blot analysis was performed to detect the expression of programmed cell death protein 4 (PDCD4) and homologous phosphatase and tensin homolog (PTEN) proteins. The levels of inflammatory factors (IL-1β, IL-6, and IL-8) and oxidative stress factors (reactive oxygen species ROS], malondialdehyde [MDA], and superoxide dismutase [SOD]) were measured using an enzyme-linked immunosorbent assay. The effect of argon on cell apoptosis was detected using flow cytometry. Argon increased the proliferation of cardiomyocytes induced by OGD, decreased the release of LDH in cell culture medium, increased miR-21 expression in cells, decreased the expression of miR-21 target proteins PDCD4 and PTEN, decreased the levels of inflammatory factors , and interleukin-8 ) and oxidative stress factors (ROS and MDA), increased the SOD content, and decreased the cell apoptosis rate. Our results suggest that argon preconditioning inhibited the PDCD4/PTEN pathway via miR-21, thereby inhibiting ROS oxidative stress and preventing MI/R injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Zhang

Shang

et al. 2021

Bioengineered

Self Cite

View full text Add to dashboard Cite

show abstract

“…Therefore, finding a new approach to prolong the survival rate of CPCs to improve the host cardiac function is an important challenge for researchers. Various approaches have been used to overcome this problem, including preconditioning stem cells by genetic or pharmacologic manipulations or exposing them to in vitro conditions that mimic the harsh environment of an ischemic heart, such as preconditioning with cobalt protoporphyrin in CSCs [21], cobalt chloride in human ESCs [22], pioglitazone in MSCs [23], argon in human cardiac myocyte-like progenitor cells [24], overexpression of Pim-1 in hCPCs [25], and pretreatment of CSCs with MSC exosome [26]. Although all of these approaches showed a potential role in improving cardiac function, the quantitative comparison of transplanted cells in the host heart and their antiapoptosis and pro-angiogenesis effect has not been demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment of cardiac progenitor cells with bradykinin attenuates H2O2-induced cell apoptosis and improves cardiac function in rats by regulating autophagy

Zhou

Qiang

et al. 2021

Stem Cell Res Ther

View full text Add to dashboard Cite

Background Previous studies have demonstrated that human cardiac c-Kit+ progenitor cells (hCPCs) can effectively improve ischemic heart disease. However, the major challenge in applying hCPCs to clinical therapy is the low survival rate of graft hCPCs in the host heart, which limited the benefit of transplanted hCPCs. Bradykinin (BK) is a principal active agent of the tissue kinin-kallikrein system. Our previous studies have highlighted that BK mediated the growth and migration of CPCs by regulating Ca2+ influx. However, the protective effect of BK on CPCs, improvement in the survival rate of BK-pretreated hCPCs in the infarcted heart, and the related mechanism remain elusive. Methods HCPCs were treated with H2O2 to induce cell apoptosis and autophagy, and different concentration of BK was applied to rescue the H2O2-induced injury detected by MTT assay, TUNEL staining, flow cytometry, western blotting, and mitoSOX assays. The role of autophagy in the anti-apoptotic effect of BK was chemically activated or inhibited using the autophagy inducer, rapamycin, or the inhibitor, 3-methyladenine (3-MA). To explore the protective effect of BK on hCPCs, 3-MA or BK-pretreated hCPCs were transplanted into the myocardial infarcted rats. An echocardiogram was used to determine cardiac function, H&E and Masson staining were employed to assess pathological characteristics, HLA gene expression was quantified by qRT-PCR, and immunostaining was applied to examine neovascularization using confocal microscopy. Results The in vitro results showed that BK suppressed H2O2-induced hCPCs apoptosis and ROS production in a concentration-dependent manner by promoting pAkt and Bcl-2 expression and reducing cleaved caspase 3 and Bax expression. Moreover, BK restrained the H2O2-induced cell autophagy by decreasing LC3II/I, Beclin1, and ATG5 expression and increasing P62 expression. In the in vivo experiment, the transplanted BK- or 3-MA-treated hCPCs were found to be more effectively improved cardiac function by decreasing cardiomyocyte apoptosis, inflammatory infiltration, and myocardial fibrosis, and promoting neovascularization in the infarcted heart, compared to untreated-hCPCs or c-kit- cardiomyocytes (CPC- cells). Conclusions Our present study established a new method to rescue transplanted hCPCs in the infarcted cardiac area via regulating cell apoptosis and autophagy of hCPCs by pretreatment with BK, providing a new therapeutic option for heart failure.

show abstract

“…The protective value of noble gases for the ex vivo preservation of organs prior to transplant and IRI during the perioperative period has been extensively verified in numerous preclinical experiments and clinical trials, with reports concerning argon and xenon being the most common (48)(49)(50)(51). In a rat spinal I/R experimental model by Liu et al (52), the rats in the I/R group with xenon-delayed post-conditioning had higher neurological scores, more normal motor neurons, fewer apoptotic neurons, and significantly higher levels of Akt and extracellular signalregulated kinase (ERK) than those without xenon-delayed post-conditioning, suggesting that xenon attenuated spinal cord IRI by activating the Akt and ERK signaling pathways.…”

Section: Noble Gasesmentioning

confidence: 99%

Novel Targets and Therapeutic Strategies to Protect Against Hepatic Ischemia Reperfusion Injury

et al. 2022

View full text Add to dashboard Cite

Hepatic ischemia reperfusion injury (IRI), a fascinating topic that has drawn a lot of interest in the last few years, is a major complication caused by a variety of clinical situations, such as liver transplantation, severe trauma, vascular surgery, and hemorrhagic shock. The IRI process involves a series of complex events, including mitochondrial deenergization, metabolic acidosis, adenosine-5'-triphosphate depletion, Kupffer cell activation, calcium overload, oxidative stress, and the upregulation of pro-inflammatory cytokine signal transduction. A number of protective strategies have been reported to ameliorate IRI, including pharmacological therapy, ischemic pre-conditioning, ischemic post-conditioning, and machine reperfusion. However, most of these strategies are only at the stage of animal model research at present, and the potential mechanisms and exact therapeutic targets have yet to be clarified. IRI remains a main cause of postoperative liver dysfunction, often leading to postoperative morbidity or even mortality. Very recently, it was reported that the activation of peroxisome proliferator-activated receptor γ (PPARγ), a member of a superfamily of nuclear transcription factors activated by agonists, can attenuate IRI in the liver, and FAM3A has been confirmed to mediate the protective effect of PPARγ in hepatic IRI. In addition, non-coding RNAs, like LncRNAs and miRNAs, have also been reported to play a pivotal role in the liver IRI process. In this review, we presented an overview of the latest advances of treatment strategies and proposed potential mechanisms behind liver IRI. We also highlighted the role of several important molecules (PPARγ, FAM3A, and non-coding RNAs) in protecting against hepatic IRI. Only after achieving a comprehensive understanding of potential mechanisms and targets behind IRI can we effectively ameliorate IRI in the liver and achieve better therapeutic effects.

show abstract

Pretreatment With Argon Protects Human Cardiac Myocyte-Like Progenitor Cells from Oxygen Glucose Deprivation-Induced Cell Death by Activation of AKT and Differential Regulation of Mapkinases

Abstract: Pretreatment with argon protects HCMs from apoptosis under ischemic conditions via activation of Akt, Erk, and biphasic regulation of JNK. Argon gas is cheap and easily administrable, and might be a novel therapy to reduce myocardial ischemia-reperfusion injury.

Cited by 13 publications

References 28 publications

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Pretreatment of cardiac progenitor cells with bradykinin attenuates H2O2-induced cell apoptosis and improves cardiac function in rats by regulating autophagy

Novel Targets and Therapeutic Strategies to Protect Against Hepatic Ischemia Reperfusion Injury

Contact Info

Product

Resources

About