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High-density lipoprotein inhibits mechanical stress-induced cardiomyocyte autophagy and cardiac hypertrophy through angiotensin II type 1 receptor-mediated PI3K/Akt pathway.

Lin L, Liu X, Xu J, Weng L, Ren J, Ge J, Zou Y - J. Cell. Mol. Med. (2015)

Bottom Line: Our results indicated that HDL significantly reduced mechanical stretch-induced rise in autophagy as demonstrated by LC3b-II and beclin-1.In addition, mechanical stress up-regulated AT1 receptor expression in both cultured cardiomyocytes and in mouse hearts, whereas HDL significantly suppressed the AT1 receptor.Furthermore, the role of Akt phosphorylation in HDL-mediated action was assessed using MK-2206, a selective inhibitor for Akt phosphorylation.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus

HDL inhibits mechanical stress-induced cardiac hypertrophy in mice. (A) BP recordings. Representative recordings from 5 mice are shown. (B) Echocardiographic analysis with representative M-mode tracings from 5 mice. Mean ± SEM from 5 mice. LVAWd: LV anterior wall thickness at end-diastole; LVPWd: LV posterior wall thickness at end-diastole; LVIDd: LV internal dimension at end-diastole; LVFS: LV fraction shortening. (C) Heart morphology and weight. Representative global heart photographs of 5 mice are shown (scale bar: 2 mm), and the heart weight to body weight ratio (HW/BW) was measured in 5 mice. (D) Haematoxylin and eosin stained LV sections of mice. The cross-sectional area (CSA) of cardiomyocytes measured using 5 sections from one heart and 5 hearts was examined (scale bar: 20 μm). (E) Expression of the ANP and SAA genes was evaluated by real-time RT-PCR. β-actin served as the internal control.
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fig03: HDL inhibits mechanical stress-induced cardiac hypertrophy in mice. (A) BP recordings. Representative recordings from 5 mice are shown. (B) Echocardiographic analysis with representative M-mode tracings from 5 mice. Mean ± SEM from 5 mice. LVAWd: LV anterior wall thickness at end-diastole; LVPWd: LV posterior wall thickness at end-diastole; LVIDd: LV internal dimension at end-diastole; LVFS: LV fraction shortening. (C) Heart morphology and weight. Representative global heart photographs of 5 mice are shown (scale bar: 2 mm), and the heart weight to body weight ratio (HW/BW) was measured in 5 mice. (D) Haematoxylin and eosin stained LV sections of mice. The cross-sectional area (CSA) of cardiomyocytes measured using 5 sections from one heart and 5 hearts was examined (scale bar: 20 μm). (E) Expression of the ANP and SAA genes was evaluated by real-time RT-PCR. β-actin served as the internal control.

Mentions: Four weeks following TAC, all mice were alive. Cardiac function and BP were examined. Our data revealed an approximate 55% rise in BP following the pressure overload procedure (Fig.3A). Echocardiographic evaluation showed that TAC-operated mice developed apparent cardiac hypertrophy, including signs of increased LV anterior wall during end diastole, LV posterior wall during end diastole, and LV internal dimension during end diastole, together with decreased LV fractional shortening (Fig.3B). Gross heart size and the ratio of heart-to-body weight (HW/BW) were also increased following pressure overload (Fig.3C). Analysis of cardiomyocyte SA in hematoxylin and eosin stained LV sections revealed that pressure overload significantly enlarged cardiomyocyte size (Fig.3D). Similar to the results from in vitro experiments, the up-regulation of SAA and ANP was also observed in the hearts from TAC-operated mice (Fig.3E).


High-density lipoprotein inhibits mechanical stress-induced cardiomyocyte autophagy and cardiac hypertrophy through angiotensin II type 1 receptor-mediated PI3K/Akt pathway.

Lin L, Liu X, Xu J, Weng L, Ren J, Ge J, Zou Y - J. Cell. Mol. Med. (2015)

HDL inhibits mechanical stress-induced cardiac hypertrophy in mice. (A) BP recordings. Representative recordings from 5 mice are shown. (B) Echocardiographic analysis with representative M-mode tracings from 5 mice. Mean ± SEM from 5 mice. LVAWd: LV anterior wall thickness at end-diastole; LVPWd: LV posterior wall thickness at end-diastole; LVIDd: LV internal dimension at end-diastole; LVFS: LV fraction shortening. (C) Heart morphology and weight. Representative global heart photographs of 5 mice are shown (scale bar: 2 mm), and the heart weight to body weight ratio (HW/BW) was measured in 5 mice. (D) Haematoxylin and eosin stained LV sections of mice. The cross-sectional area (CSA) of cardiomyocytes measured using 5 sections from one heart and 5 hearts was examined (scale bar: 20 μm). (E) Expression of the ANP and SAA genes was evaluated by real-time RT-PCR. β-actin served as the internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549043&req=5

fig03: HDL inhibits mechanical stress-induced cardiac hypertrophy in mice. (A) BP recordings. Representative recordings from 5 mice are shown. (B) Echocardiographic analysis with representative M-mode tracings from 5 mice. Mean ± SEM from 5 mice. LVAWd: LV anterior wall thickness at end-diastole; LVPWd: LV posterior wall thickness at end-diastole; LVIDd: LV internal dimension at end-diastole; LVFS: LV fraction shortening. (C) Heart morphology and weight. Representative global heart photographs of 5 mice are shown (scale bar: 2 mm), and the heart weight to body weight ratio (HW/BW) was measured in 5 mice. (D) Haematoxylin and eosin stained LV sections of mice. The cross-sectional area (CSA) of cardiomyocytes measured using 5 sections from one heart and 5 hearts was examined (scale bar: 20 μm). (E) Expression of the ANP and SAA genes was evaluated by real-time RT-PCR. β-actin served as the internal control.
Mentions: Four weeks following TAC, all mice were alive. Cardiac function and BP were examined. Our data revealed an approximate 55% rise in BP following the pressure overload procedure (Fig.3A). Echocardiographic evaluation showed that TAC-operated mice developed apparent cardiac hypertrophy, including signs of increased LV anterior wall during end diastole, LV posterior wall during end diastole, and LV internal dimension during end diastole, together with decreased LV fractional shortening (Fig.3B). Gross heart size and the ratio of heart-to-body weight (HW/BW) were also increased following pressure overload (Fig.3C). Analysis of cardiomyocyte SA in hematoxylin and eosin stained LV sections revealed that pressure overload significantly enlarged cardiomyocyte size (Fig.3D). Similar to the results from in vitro experiments, the up-regulation of SAA and ANP was also observed in the hearts from TAC-operated mice (Fig.3E).

Bottom Line: Our results indicated that HDL significantly reduced mechanical stretch-induced rise in autophagy as demonstrated by LC3b-II and beclin-1.In addition, mechanical stress up-regulated AT1 receptor expression in both cultured cardiomyocytes and in mouse hearts, whereas HDL significantly suppressed the AT1 receptor.Furthermore, the role of Akt phosphorylation in HDL-mediated action was assessed using MK-2206, a selective inhibitor for Akt phosphorylation.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus