Hsa-miR-199a-5p Protect Cell Injury in Hypoxia Induces Myocardial Cells Via Targeting HIF1α

2021 ◽  
Author(s):  
Hui-Yong Chen ◽  
Jun Lu ◽  
Zheng-Kang Wang ◽  
Jie Yang ◽  
Xiao Ling ◽  
...  
Keyword(s):  
Cell Injury ◽  
Myocardial Cells

Reduced arachidonate metabolism in ATP-depleted myocardial cells occurs early in cell injury

1990 ◽  
Vol 259 (2) ◽  
pp. H582-H591 ◽  
Author(s):  
G. E. Revtyak ◽  
L. M. Buja ◽  
K. R. Chien ◽  
W. B. Campbell
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Cell Injury ◽  
Arachidonic Acid Metabolism ◽  
Atp Depletion ◽  
Neonatal Rat ◽  
Eicosatetraenoic Acid ◽  
Metabolic Inhibitors ◽  
Early Event ◽  
Myocardial Cells

Exposure of cultured neonatal rat myocardial cells to metabolic inhibitors results in cellular ATP depletion. If prolonged, arachidonic acid is released from membrane phospholipid and irreversible cell injury may ensue. The present study was undertaken to identify the major products of arachidonic acid formed when myocardial cells are depleted of ATP by the metabolic inhibitors 2-deoxy-D-glucose (2-DG) and oligomycin (OG). Under basal conditions, myocardial cells metabolize [3H]arachidonic acid to 6-keto-[3H]prostaglandin (PG)F1 alpha, [3H]PGE2, [3H]PGF2 alpha, 12-[3H]hydroxy-6,8,11,14-eicosatetraenoic acid (12-[3H]HETE) and 11-[3H]HETE, indicating that these cells contain both cyclooxygenase and lipoxygenase pathways. After exposure of myocardial cells to 10 mM 2-DG and 0.1 micrograms/ml OG for 4 h, the basal release of 6-keto-PGF1 alpha and PGE2 is reduced by 3.4-fold and 2-fold, respectively. Supernatants obtained from cells prelabeled with [3H]arachidonic acid and treated with 2-DG and OG for 4 or 12 h did not contain detectable [3H]prostaglandins or [3H]HETEs, but only [3H]arachidonic acid when compared with untreated cells. After 4 and 12 h of treatment with 2-DG and OG, there was a 3.4- and 4.4-fold net release of endogenous arachidonic acid from treated compared with untreated cells. When stimulated with bradykinin, melittin (a phospholipase activator), or arachidonic acid, the synthesis of 6-keto-PGF1 alpha increased to a similar extent in both 2-DG- and OG-treated and -untreated cells. Hence, ATP-depleted myocardial cells do not convert arachidonic acid to oxygenated metabolites under basal conditions. The reduced arachidonic acid metabolism during ATP depletion is not due to direct inactivation of cyclooxygenase or membrane phospholipase. This impairment in arachidonic acid metabolism may represent an early event in myocardial cell injury.

Cell injury of cultured rat myocardial cells after reoxygenation of hypoxic cultures in the presence and absence of calcium

In Vitro ◽  
1984 ◽  
Vol 20 (8) ◽  
pp. 642-646 ◽  
Author(s):  
Daniel Acosta ◽  
Kenneth Ramos ◽  
Cheng-Pei Li-Goldman
Keyword(s):  
Cell Injury ◽  
Myocardial Cells ◽  
Presence And Absence

scholarly journals Role of Thrombospondin-1 in Sepsis-Induced Myocardial Injury

2021 ◽  
Author(s):  
YUN XIE ◽  
JIAXIANG ZHANG ◽  
WEI JIN ◽  
RUI TIAN ◽  
Ruilan Wang
Keyword(s):  
Mrna Expression ◽  
Real Time ◽  
Quantitative Pcr ◽  
Myocardial Injury ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Expression Level ◽  
Myocardial Cells ◽  
Thrombospondin 1 ◽  
Myocardial Cell Injury

Abstract Objective: Sepsis often causes myocardial injury with a high mortality. We wanted to investigate the effects of thrombospondin-1 (THBS1) expression on myocardial cell injury, oxidative stress and apoptosis in sepsis.Methods: The expression of THBS1 mRNA in LPS-induced mouse primary cardiomyocytes was detected by real-time fluorescence quantitative PCR. We constructed a eukaryotic siRNA expression vector and used liposome transfection to knockdown THBS1 mRNA expression in myocardial cells. We detected the THBS1 mRNA expression level using real-time fluorescent quantitative PCR. Four groups were used: control, LPS, THBS1 siRNA, and LPS + THBS1 siRNA. ELISA was used to detect cTnI, proBNP, ROS, caspase3 and other indicators of cell damage. At the same time, sepsis mouse models were prepared for H&E, TUNEL and caspase-3 staining to evaluate myocardial cell injury and apoptosis. Clinical samples were collected to analyze the serum THBS1 level and correlate it with the prognosis of patients with myocardial injury of sepsis.Results: The expression level of THBS1 mRNA in myocardial cells induced by LPS was increased, and the serum THBS1 level in patients with myocardial injury in sepsis was also significantly increased. In the THBS1 siRNA group with myocardial injury, the levels of cTnI and proBNP were significantly decreased, the levels of the inflammatory cytokines IL-6 and TNF-α were significantly decreased, ROS were significantly decreased, and caspase3 was significantly decreased, and myocardial cell apoptosis was also reduced in the sepsis mouse model. Conclusion: THBS1 is closely related to the biological behavior of myocardial cells and may be a therapeutic target for myocardial injury in sepsis.

scholarly journals Astragaloside IV Reduces OxLDL-Induced BNP Overexpression by Regulating HDAC

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Wenting Zhang ◽  
Xin Wang ◽  
Jing Li ◽  
Mingyuan Xu ◽  
Xiaolu Ren ◽  
...  
Keyword(s):  
Treatment Group ◽  
Immunosorbent Assay ◽  
Protein Level ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Myocardial Cells ◽  
Astragaloside Iv ◽  
Hdac Activity ◽  
Myocardial Cell Injury

Effective drug intervention is the most important method to improve the prognosis, improve the quality of life, and prolong the life of patients with heart failure. This study aimed to explore the protective effect of astragaloside IV on myocardial cell injury induced by oxidized low-density lipoprotein (OxLDL) and its regulatory mechanism on the increase of brain natriuretic peptide (BNP) caused by myocardial cell injury. The model of myocardial cell injury, protection, and histone deacetylase (HDAC) inhibition in HL-1 mice was established by OxLDL treatment, astragaloside IV intervention, and UF010 coincubation. The effects of OxLDL and astragaloside IV on apoptosis were detected by flow cytometry. The expression level of BNP mRNA and protein in cells was investigated by real-time fluorescence quantification, western blot, and enzyme-linked immunosorbent assay. HDAC activity in nucleus was calibrated by fluorescence absorption intensity. Enzyme-linked immunosorbent assay (ELISA) was applied to test eNOS level in myocardial cells. OxLDL significantly promoted apoptosis, upregulated BNP mRNA, increased BNP protein level inside and outside cells, and decreased eNOS level. Compared with OxLDL treatment group, apoptosis decreased, BNP mRNA expression level decreased, BNP protein concentration decreased, and eNOS level increased significantly combined with low and high concentration astragaloside IV treatment group. HDAC activity significantly increased in OxLDL treatment group and significantly decreased after combined incubation with low and high concentrations of astragaloside IV. Inhibition of HDAC significantly increased eNOS level and decreased BNP protein level. In conclusion, astragaloside IV can reverse the low level of eNOS caused by OxLDL by regulating HDAC activity to protect myocardial cells from oxide damage, which is manifested by the decrease of BNP concentration.

scholarly journals Dexmedetomidine Postconditioning Alleviates Hypoxia/Reoxygenation Injury in Senescent Myocardial Cells by Regulating lncRNA H19 and m6A Modification

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Xuan Zhang ◽  
Qiang Fu ◽  
Longhe Xu ◽  
Yitian Yang ◽  
Weixing Zhao ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Cell ◽  
Rna Modification ◽  
H9c2 Cell ◽  
H9c2 Cells ◽  
Myocardial Cells ◽  
Apoptosis Protein ◽  
Hypoxia Reoxygenation

H19, a long noncoding RNA (lncRNA), reportedly protects myocardial cells (H9c2 cell line) against hypoxia-reoxygenation- (H/R-) induced injury. Dexmedetomidine (Dex) has an important myocardial protective effect, although its function and mechanism in cardiac ischemia/reperfusion (I/R) injury, especially for senile patients, requires further study. RNA N6-methyladenosine (m6A) is the most abundant endogenous RNA modification. However, the effect of Dex postconditioning on RNA m6A modification has rarely been reported. The aim of this study was to evaluate roles of H19 and m6A modification in Dex postconditioning of aged cardiomyocytes. Hydrogen peroxide (H2O2) was used to induce senescence of H9c2 cells. After 6 h of hypoxia, H9c2 cells were exposed to different concentrations of dexmedetomidine (0, 500 nM, 1 μM, and 2 μM) for 6 h. After knockdown or overexpression of H19 and its downstream gene miR-29b-3p and cellular inhibitor of apoptosis protein 1 (cIAP1), Dex postconditioning experiments were performed to examine effects on myocardial cell injury. Global m6A levels after H/R with or without Dex postconditioning were measured with a colorimetric m6A RNA Methylation Quantification Kit. The mechanism by which RNA m6A methylation regulated genes mediating H19 expression was verified by m6A RNA immunoprecipitation (MeRIP), and the function of Dex postconditioning of aged cardiomyocytes was investigated. Dex postconditioning protected against H/R-induced injury of aged myocardial cells through H19/miR-29b-3p/cIAP1, increased methylation of RNA m6A elicited by H/R, and attenuated H/R-induced injury by suppressing expression of the RNA m6A demethylase gene alkB homolog 5 (ALKBH5). In addition, AKLBH5 regulated the expression of H19, and Dex postconditioning attenuated H/R-induced injury via ALKBH5 in aged cardiomyocytes.

scholarly journals Protective Effect of Tetramethylpyrazine on Myocardial Ischemia-Reperfusion Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Weidong Qian ◽  
Xingjiang Xiong ◽  
Zhuyuan Fang ◽  
Haiting Lu ◽  
Zhensheng Wang
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Research Progress ◽  
Protective Effects ◽  
Myocardial Cells ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia-reperfusion injury (MIRI) is a common pathological and physiological phenomenon. Tetramethylpyrazine is the extract of the traditional Chinese medicine Chuanxiong, which can exert protective effects on MIRI in multiple ways. This paper reviewed the current research progress and evidence about the cardiovascular effects of tetramethylpyrazine, which included protecting mitochondria and improving energy metabolism, scavenging oxygen free radicals (OFRs) to inhibit lipid peroxidation, attenuating calcium (Ca2+) overload and maintaining Ca2+homeostasis in cells, inhibiting apoptosis and protecting myocardial cells, interfering with the inflammatory reaction and mitigating cell injury, interfering with cell signaling pathways, and improving function of endothelial cells and protecting myocardial cells. However, further rigorously designed randomized controlled trials are warranted.

Reduction of cell injury in hypoxic cultures of rat myocardial cells by methylprednisolone

In Vitro ◽  
1980 ◽  
Vol 16 (2) ◽  
pp. 93-96 ◽  
Author(s):  
Daniel Acosta ◽  
Marianne Puckett ◽  
Cheng-Pei Li
Keyword(s):  
Cell Injury ◽  
Myocardial Cells

The Ultrastructure of Myocardial Cells in Normal and Cardiac Lethal Mutant Mexican Axolotls, (Ambystoma Mexicanum)

1970 ◽  
Vol 28 ◽  
pp. 62-63
Author(s):  
Larry F. Lemanski ◽  
Eldridge M. Bertke ◽  
J. T. Justus
Keyword(s):  
Fine Structure ◽  
Heart Development ◽  
Osmium Tetroxide ◽  
Picric Acid ◽  
Ambystoma Mexicanum ◽  
Recessive Mutation ◽  
Acid Mixture ◽  
Myocardial Cells ◽  
Lethal Mutant ◽  
Mexican Axolotl

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.

Immunocytochemical localization of desmin and vimentin in chick embryonic myocardial cells

1990 ◽  
Vol 48 (3) ◽  
pp. 448-449
Author(s):  
Yukiko Sugi
Keyword(s):  
Sodium Methoxide ◽  
Intermediate Filament Protein ◽  
Chick Embryos ◽  
Immunocytochemical Localization ◽  
Myocardial Cells ◽  
Immunofluorescence Study ◽  
Immunofluorescent Localization ◽  
Rabbit Igg ◽  
Semithin Sections ◽  
Filament Protein

In cultured skeletal muscle cells of chick, one intermediate filament protein, vimentin, is primarily formed and then synthesis of desmin follows. Coexistence of vimentin and desmin has been immunocytochemically confirmed in chick embryonic skeletal musclecells. Immunofluorescent localization of vimentin and desmin has been described in developing myocardial cells of hamster. However, initial localization of desmin and vimentin in early embryonic heart has not been reported in detail. By quick-freeze deep-etch method a loose network of intermediate filaments was revealed to exist surrounding myofibrils. In this report, immunocytochemical localization of desmin and vimentin is visualized in early stages of chick embryonic my ocardium.Chick embryos, Hamburger-Hamilton (H-H) stage 8 to hatch, and 1 day old postnatal chicks were used in this study. For immunofluorescence study, each embryo was fixed with 4% paraformaldehyde and embedded in Epon 812. De-epoxinized with sodium methoxide, semithin sections were stained with primary antibodies (rabbit anti-desmin antibody and anti-vimentin antibody)and secondary antibody (RITC conjugated goat-anti rabbit IgG).

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