A Comorbidity Model of Myocardial Ischemia/Reperfusion Injury and Hypercholesterolemia in Rat Cardiac Myocyte Cultures

Makkos, András; Szántai, Á.; Pálóczi, János; Pipis, Judit; Kiss, Bernadett; Poggi, Paola; Ferdinándy, Péter; Chatgilialoglu, Alexandros; Görbe, Anikó

doi:10.3389/fphys.2019.01564

Cited by 21 publications

(15 citation statements)

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“…The protocol using three alternating cycles of 5 minutes of ischemia and reperfusion was chosen, because it was extensively studied in perconditioning research 1 , 26 - 29 , showing promisors results in hepatic, renal and cardiac IR. Costa et al .…”

Section: Discussionmentioning

confidence: 99%

Remote ischemic conditioning improves rat brain antioxidant defense in a time-dependent mechanism

et al. 2021

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Purpose To clarify the best protocol for performing remote ischemic conditioning and to minimize the consequences of ischemia and reperfusion syndrome in brain, the present study aimed to evaluate different time protocols and the relation of the organs and the antioxidant effects of this technique. Methods The rat’s left femoral artery was clamped with a microvascular clamp in times that ranged from 1 to 5 minutes, according to the corresponding group. After the cycles of remote ischemic conditioning and a reperfusion of 20 minutes, the brain and the left gastrocnemius were collected. The samples were used to measure glutathione peroxidase, glutathione reductase and catalase levels. Results In the gastrocnemius, the 4-minute protocol increased the catalase concentration compared to the 1-minute protocol, but the latter increased both glutathione peroxidase and glutathione reductase compared to the former. On the other hand, the brain demonstrated higher catalase and glutathione peroxidase in 5-minute group, and the 3-minute group reached higher values of glutathione reductase. Conclusions Remote ischemic conditioning increases brain antioxidant capacity in a time-dependent way, while muscle presents higher protection on 1-minute cycles and tends to decrease its defence with longer cycles of intermittent occlusions of the femoral artery.

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Section: Discussionmentioning

confidence: 99%

Remote ischemic conditioning improves rat brain antioxidant defense in a time-dependent mechanism

et al. 2021

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“…In vitro disease modeling of myocardial I/R injury allows the use of isolated cardiac cells from either human or animal origin to mimic changes in oxygen levels (hypoxia/normoxia), typical of the ischemic and reperfused states of an infarcted heart. To date, cells used in in vitro disease models of myocardial I/R injury include: i) cultures of primary cardiomyocytes; [53][54][55][56] ii) inducedpluripotent-stem-cell (iPSC)-derived cardiac cells; [57,58] iii) cardiac cell lines; [59][60][61][62][63][64] and iv) cardiac progenitor cells. [65,66] These cells have been primarily used in 2D monolayer culture, while in some cases these were employed in 3D cultures.…”

Section: In Vitro Myocardial I/r Injury Modelsmentioning

confidence: 99%

Considerations for the Bioengineering of Advanced Cardiac In Vitro Models of Myocardial Infarction

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et al. 2021

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Despite the latest advances in cardiovascular biology and medicine, myocardial infarction (MI) remains one of the major causes of deaths worldwide. While reperfusion of the myocardium is critical to limit the ischemic damage typical of a MI event, it causes detrimental morphological and functional changes known as “reperfusion injury.” This complex scenario is poorly represented in currently available models of ischemia/reperfusion injury, leading to a poor translation of findings from the bench to the bedside. However, more recent bioengineered in vitro models of the human heart represent more clinically relevant tools to prevent and treat MI in patients. These include 3D cultures of cardiac cells, the use of patient‐derived stem cells, and 3D bioprinting technology. This review aims at highlighting the major features typical of a heart attack while comparing current in vitro, ex vivo, and in vivo models. This information has the potential to further guide in developing novel advanced in vitro cardiac models of ischemia/reperfusion injury. It may pave the way for the generation of advanced pathophysiological cardiac models with the potential to develop personalized therapies.

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“…The primary culture of adult rat cardiomyocytes was prepared as described previously (Makkos et al, 2019). Briefly, male Wistar rats (150-200 g) were anesthetized with pentobarbital (60 mg/kg) and heparinized (500 IU/kg).…”

Section: Cardiac Cell Culturesmentioning

confidence: 99%

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

et al. 2021

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Little is known about the role of the neuropeptide somatostatin (SST) in myocardial ischemia/reperfusion injury and cardioprotection. Here, we investigated the direct cardiocytoprotective effect of SST on ischemia/reperfusion injury in cardiomyocyte cultures, as well as the expression of SST and its receptors in pig and human heart tissues. SST induced a bell-shaped, concentration-dependent cardiocytoprotection in both adult rat primary cardiomyocytes and H9C2 cells subjected to simulated ischemia/reperfusion injury. Furthermore, in a translational porcine closed-chest acute myocardial infarction model, ischemic preconditioning increased plasma SST-like immunoreactivity. Interestingly, SST expression was detectable at the protein, but not at the mRNA level in the pig left ventricles. SSTR1 and SSTR2, but not the other SST receptors, were detectable at the mRNA level by PCR and sequencing in the pig left ventricle. Moreover, remote ischemic conditioning upregulated SSTR1 mRNA. Similarly, SST expression was also detectable in healthy human interventricular septum samples at the protein level. Furthermore, SST-like immunoreactivity decreased in interventricular septum samples of patients with ischemic cardiomyopathy. SSTR1, SSTR2, and SSTR5 but not SST and the other SST receptors were detectable at the mRNA level by sequencing in healthy human left ventricles. In addition, in healthy human left ventricle samples, SSTR1 and SSTR2 mRNAs were expressed especially in vascular endothelial and some other cell types as detected by RNA Scope®in situ hybridization. This is the first demonstration that SST exerts a direct cardiocytoprotective effect against simulated ischemia/reperfusion injury. Moreover, SST is expressed in the heart tissue at the peptide level; however, it is likely to be of sensory neural origin since its mRNA is not detectable. SSTR1 and SSTR2 might be involved in the cardioprotective action of SST, but other mechanisms cannot be excluded.

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A Comorbidity Model of Myocardial Ischemia/Reperfusion Injury and Hypercholesterolemia in Rat Cardiac Myocyte Cultures

Cited by 21 publications

References 54 publications

Remote ischemic conditioning improves rat brain antioxidant defense in a time-dependent mechanism

Remote ischemic conditioning improves rat brain antioxidant defense in a time-dependent mechanism

Considerations for the Bioengineering of Advanced Cardiac In Vitro Models of Myocardial Infarction

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

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