"Malignant" right coronary artery presenting as an ST-segment elevation myocardial infarction-a case report.

Figures

• 

  Figure 1.. CRP aggravated myocardial IRI. (A): The cardiomyocytes incubated with 10 µg/mL of CRP before OGD have a significant effect on IRI; (B): immunofluorescence staining of neonatal rat cardiomyocytes with anti-α-actin antibody (red) and DAPI for nuclei (blue); (C): analysis of the effect of CRP on cell viability, detected by MTS assay; (D): effect of CRP on LDH levels in primary cardiomyocytes after OGD/R. Data were presented as mean ± SD. ★P < 0.05 compared with the control group; #P < 0.05 compared with OGD/R group. CRP: C-reactive protein; IRI: ischemia reperfusion injury; LDH: lactate dehydrogenase; MTS: 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reoxygenation.

• 

  Figure 2.. CRP promoted the opening of mPTP. (A): effect of CRP on the calcein fluorescence by confocal laser scanning microscope. Compared with control group, OGD/R significantly reduced the intensity of fluorescence. The pretreatment with CRP (10 µg/mL) for 24 hours further decreased fluorescence intensity significantly. (B): the specific values of calcein/AM fluorescent intensities in above groups were shown. Data were presented as mean ± SD. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group. AM: aminomethyl; CRP: C-reactive protein; mPTP: mitochondrial permeability transition pores; OGD/R: oxygen-glucose deprivation/reoxygenation.

• 

  Figure 3.. CRP aggravated depolarization of mitochondrial membrane potential in cardiomyocytes. (A): effect of CRP on the TMRE fluorescence by confocal laser scanning microscope. Compared with control group, OGD/R significantly reduced the intensity of fluorescence. The pretreatment with CRP (10 µg/mL) for 24 hours further decreased fluorescence intensity significantly. (B): the specific values of TMRE fluorescent intensities in above groups were shown. Data were presented as mean ± SD. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group. CRP: C-reactive protein; OGD/R: oxygen-glucose deprivation/ reoxygenation; TMRE: tetramethylrhodamine ethyl ester.

• 

  Figure 4.. Ator protected cardiomyocytes from CRP-mediated IRI. (A): analysis of the effects of Ator, CsA and DZ on cell viability, detected by MTS assay. SD rat cardiomyocytes were incubated with CRP at concentration of 10 µg/mL for 24 hours, aggravating cell injury induced by OGD/R. This adverse effect of CRP was blocked by CsA (10 µM) or DZ (100 µM). Ator (1 µM) preconditioned primary cardiomyocytes against CRP-induced cell injury. (B); effects of Ator, CsA and DZ on LDH level in primary cardiomyocytes after OGD/R. Data were presented as mean ± SD. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group; ▴P < 0.05 compared with CRP+OGD/R group. Ator: Atorvastatin; CRP: C-reactive protein; CsA: cyclosporin A; DZ: diazoxide; IRI: ischemia reperfusion injury; LDH: lactate dehydrogenase; OGD/R: oxygen-glucose deprivation/reoxygenation.

• 

  Figure 5.. Ator alleviated mPTP opening in cardiomyocytes. (A): effect of Ator on the calcein fluorescence by confocal laser scanning microscope. Pretreatment with Ator (1 µM) for three hours resulted in a significant increase in fluorescence intensity. In addition, CsA (10 µM) or DZ (100 µM) inhibited the CRP-induced decrease of fluorescence intensity. (B): the specific values of calcein/AM fluorescent intensities in above groups were shown. Data were presented as mean ± SD. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group; ▴P < 0.05 compared with CRP + OGD/R group. AM: aminomethyl; Ator: Atorvastatin; CRP: C-reactive protein; CsA: cyclosporin A; DZ: diazoxide; mPTP: permeability transition pores; OGD/R: oxygen-glucose deprivation/reoxygenation.

• 

  Figure 6.. Ator prevented depolarization of mitochondrial membrane potential in cardiomyocytes. (A): effect of Ator on the TMRE fluorescence by confocal laser scanning microscope. Compared with CRP + OGD/R group, the pretreatment with Ator (1 µM) for three hours resulted in a significant increase in fluorescence intensity. In addition, cotreatment with CsA (10 µM) or DZ (100 µM) inhibited the CRP-induced decrease of fluorescence intensity. (B): the specific values of calcein/AM fluorescent intensities in above groups were shown. Data were presented as mean ± SD. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group; ▴P < 0.05 compared with CRP + OGD/R group. AM: aminomethyl; Ator: Atorvastatin; CRP: C-reactive protein; CsA: cyclosporin A; DZ: diazoxide; OGD/R: oxygen-glucose deprivation/ reoxygenation; TMRE: tetramethylrhodamine ethyl ester.

• 

  Figure 7.. Analysis of the effects of CRP and Ator on related protein expressions, detected by western blot. β-actin was used as a loading control. These results indicated that CRP aggravated myocardial ischemia reperfusion mainly via activating the ERK signaling pathway, and Atorvastatin protected cardiomyocytes from CRP-induced ischemia reperfusion through the Akt and ERK Signaling Pathway. ★P < 0.05 compared with control group; #P < 0.05 compared with OGD/R group; ▴P < 0.05 compared with CRP + OGD/R group. Ator: Atorvastatin; CRP: C-reactive protein; ERK: extracellular-signal-regulated kinase; JNK: Jun N-terminal kinase; MAPK: mitogen activated protein kinase; OGD/R: oxygen-glucose deprivation/ reoxygenation; p-ERK.

• 

  Figure 8.. The schematic diagram of the related mechanisms involved in the CRP-induced ischemia reperfusion injury in cardiomyocytes. CRP: C-reactive protein; ERK: extracellular-signal-regulated kinase; mitoKATP: mitochondrial ATP-sensitive potassium; mPTP: permeability transition pores.