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Parkin Regulates Mitochondrial Autophagy After Myocardial Infarction in Rats.

Wu L, Maimaitirexiati X, Jiang Y, Liu L - Med. Sci. Monit. (2016)

Bottom Line: After MI, increased numbers of mitochondria and autophagosomes were observed in the myocardium (p<0.05), and the mitochondrial morphology was destroyed.In addition, the levels of the autophagy-related proteins LC3II/LC3I were elevated in the myocardium after MI (p<0.05) and the activity of Parkin was significantly reduced (p<0.05).CONCLUSIONS Under conditions of chronic MI, mitochondrial dysfunction and disruption of autophagosomal clearance are associated with Parkin expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Unit, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).

ABSTRACT
BACKGROUND To study the role of Parkin in the regulation of mitochondrial autophagy in the heart by assessing mitochondrial autophagy and changes in Parkin protein expression in rat myocardium after myocardial infarction (MI). MATERIAL AND METHODS Rats were randomly assigned to three groups: control, sham, and MI. Four weeks after induction of MI, ultrasonic examination of the rats was performed to measure left ventricular end systolic diameter (LVESD), left ventricular end diastolic diameter (LVEDD), left ventricular ejection fraction (EF), left ventricular fractional shortening (FS), and left ventricular diastolic/systolic volume. Rat myocardium was collected from each group and examined for changes in morphology, size, and amount of mitochondria and autophagosomes by transmission electronic microscopy. A Western blot was performed to analyze the levels of Parkin and the autophagy-related protein LC3. RESULTS Four weeks after MI, cardiac function of the MI rats was impaired compared with the control rats. Both LVESD and LVEDD were elevated in the MI rats (p<0.05) while EF was decreased, indicating that the MI model was constructed successfully. After MI, increased numbers of mitochondria and autophagosomes were observed in the myocardium (p<0.05), and the mitochondrial morphology was destroyed. Chloroquine (CQ) treatment increased the number of autophagosomes in the myocardium of the control rats (p<0.05) but not in MI rats (p>0.05). In addition, the levels of the autophagy-related proteins LC3II/LC3I were elevated in the myocardium after MI (p<0.05) and the activity of Parkin was significantly reduced (p<0.05). CONCLUSIONS Under conditions of chronic MI, mitochondrial dysfunction and disruption of autophagosomal clearance are associated with Parkin expression.

No MeSH data available.


Related in: MedlinePlus

Relative expression of LC3II/LC3I in the myocardium of control, sham, and MI groups. * p<0.05 when comparing MI and control group.
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f4-medscimonit-22-1553: Relative expression of LC3II/LC3I in the myocardium of control, sham, and MI groups. * p<0.05 when comparing MI and control group.

Mentions: Myocardial tissue from the left ventricle was obtained from the rats of the control, sham, and MI groups, and the activity of LC3 I/II was determined. As shown in Figure 4, the LC3 II/LC3 I ratio was higher in the MI group than in the control group (p<0.05), suggesting that MI could induce the conversion of LC3 I to LC3 II, and thus increase the level of LC3 II.


Parkin Regulates Mitochondrial Autophagy After Myocardial Infarction in Rats.

Wu L, Maimaitirexiati X, Jiang Y, Liu L - Med. Sci. Monit. (2016)

Relative expression of LC3II/LC3I in the myocardium of control, sham, and MI groups. * p<0.05 when comparing MI and control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4920096&req=5

f4-medscimonit-22-1553: Relative expression of LC3II/LC3I in the myocardium of control, sham, and MI groups. * p<0.05 when comparing MI and control group.
Mentions: Myocardial tissue from the left ventricle was obtained from the rats of the control, sham, and MI groups, and the activity of LC3 I/II was determined. As shown in Figure 4, the LC3 II/LC3 I ratio was higher in the MI group than in the control group (p<0.05), suggesting that MI could induce the conversion of LC3 I to LC3 II, and thus increase the level of LC3 II.

Bottom Line: After MI, increased numbers of mitochondria and autophagosomes were observed in the myocardium (p<0.05), and the mitochondrial morphology was destroyed.In addition, the levels of the autophagy-related proteins LC3II/LC3I were elevated in the myocardium after MI (p<0.05) and the activity of Parkin was significantly reduced (p<0.05).CONCLUSIONS Under conditions of chronic MI, mitochondrial dysfunction and disruption of autophagosomal clearance are associated with Parkin expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Unit, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).

ABSTRACT
BACKGROUND To study the role of Parkin in the regulation of mitochondrial autophagy in the heart by assessing mitochondrial autophagy and changes in Parkin protein expression in rat myocardium after myocardial infarction (MI). MATERIAL AND METHODS Rats were randomly assigned to three groups: control, sham, and MI. Four weeks after induction of MI, ultrasonic examination of the rats was performed to measure left ventricular end systolic diameter (LVESD), left ventricular end diastolic diameter (LVEDD), left ventricular ejection fraction (EF), left ventricular fractional shortening (FS), and left ventricular diastolic/systolic volume. Rat myocardium was collected from each group and examined for changes in morphology, size, and amount of mitochondria and autophagosomes by transmission electronic microscopy. A Western blot was performed to analyze the levels of Parkin and the autophagy-related protein LC3. RESULTS Four weeks after MI, cardiac function of the MI rats was impaired compared with the control rats. Both LVESD and LVEDD were elevated in the MI rats (p<0.05) while EF was decreased, indicating that the MI model was constructed successfully. After MI, increased numbers of mitochondria and autophagosomes were observed in the myocardium (p<0.05), and the mitochondrial morphology was destroyed. Chloroquine (CQ) treatment increased the number of autophagosomes in the myocardium of the control rats (p<0.05) but not in MI rats (p>0.05). In addition, the levels of the autophagy-related proteins LC3II/LC3I were elevated in the myocardium after MI (p<0.05) and the activity of Parkin was significantly reduced (p<0.05). CONCLUSIONS Under conditions of chronic MI, mitochondrial dysfunction and disruption of autophagosomal clearance are associated with Parkin expression.

No MeSH data available.


Related in: MedlinePlus