Limits...
RNA interference of myocyte enhancer factor 2A accelerates atherosclerosis in apolipoprotein E-deficient mice.

Zhou WP, Zhang H, Zhao YX, Liu GQ, Zhang JY - PLoS ONE (2015)

Bottom Line: Myocyte enhancer factor-2A (MEF 2A) has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear.Six weeks after surgery, lentiviral shRNA construct was used to silence the expression of MEF 2A.The expression level of MEF 2A was significantly reduced in plasma and plaque in the RNAi group, compared to the control and NC groups, whereas the expression level of pro-inflammatory cytokines was markedly increased.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.

ABSTRACT

Objective: Myocyte enhancer factor-2A (MEF 2A) has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear. In the present study we aim to assess the role of MEF 2A in the progression of pre-existing atherosclerosis.

Methods: Eighty apolipoprotein E-deficient mice (APOE KO) were randomly allocated to control, scramble and MEF 2A RNA interference (RNAi) groups, and constrictive collars were used to induce plaque formation. Six weeks after surgery, lentiviral shRNA construct was used to silence the expression of MEF 2A. Carotid plaques were harvested for analysis 4 weeks after viral vector transduction. Inflammatory gene expression in the plasma and carotid plaques was determined by using ELISAs and real-time RT-PCR.

Results: The expression level of MEF 2A was significantly reduced in plasma and plaque in the RNAi group, compared to the control and NC groups, whereas the expression level of pro-inflammatory cytokines was markedly increased. Silencing MEF 2A using lentiviral shRNA significantly reduced the plaque collagen content and fibrous cap thickness, as well as increased plaque area. However, silencing MEF 2A had no obvious effect on plaque lipid content.

Conclusions: Lentivirus-mediated MEF 2A shRNA accelerates inflammation and atherosclerosis in APOE KO mice, but has no effect on lipoprotein levels in plasma.

No MeSH data available.


Related in: MedlinePlus

Efficiency of lentviral shRNA vector transduction in the carotid plaques.A, B, C. GFP expression in sections of the carotid plaques was imaged from NC group. Carotid plaques at 1, 2 and 4 weeks following transduction were visualized under fluorescent microscope. (200×).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4368513&req=5

pone.0121823.g003: Efficiency of lentviral shRNA vector transduction in the carotid plaques.A, B, C. GFP expression in sections of the carotid plaques was imaged from NC group. Carotid plaques at 1, 2 and 4 weeks following transduction were visualized under fluorescent microscope. (200×).

Mentions: Previous studies [14] have indicated that GFP expression provided an efficient and convenient approach to detect the efficiency of transduction. GFP fluorescence in carotid plaques was observed one week after transduction. The strongest GFP fluorescence was displayed two weeks after transduction (Fig. 3A-C), demonstrating that lentivirus can efficiently transduce plaques in vivo.


RNA interference of myocyte enhancer factor 2A accelerates atherosclerosis in apolipoprotein E-deficient mice.

Zhou WP, Zhang H, Zhao YX, Liu GQ, Zhang JY - PLoS ONE (2015)

Efficiency of lentviral shRNA vector transduction in the carotid plaques.A, B, C. GFP expression in sections of the carotid plaques was imaged from NC group. Carotid plaques at 1, 2 and 4 weeks following transduction were visualized under fluorescent microscope. (200×).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4368513&req=5

pone.0121823.g003: Efficiency of lentviral shRNA vector transduction in the carotid plaques.A, B, C. GFP expression in sections of the carotid plaques was imaged from NC group. Carotid plaques at 1, 2 and 4 weeks following transduction were visualized under fluorescent microscope. (200×).
Mentions: Previous studies [14] have indicated that GFP expression provided an efficient and convenient approach to detect the efficiency of transduction. GFP fluorescence in carotid plaques was observed one week after transduction. The strongest GFP fluorescence was displayed two weeks after transduction (Fig. 3A-C), demonstrating that lentivirus can efficiently transduce plaques in vivo.

Bottom Line: Myocyte enhancer factor-2A (MEF 2A) has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear.Six weeks after surgery, lentiviral shRNA construct was used to silence the expression of MEF 2A.The expression level of MEF 2A was significantly reduced in plasma and plaque in the RNAi group, compared to the control and NC groups, whereas the expression level of pro-inflammatory cytokines was markedly increased.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.

ABSTRACT

Objective: Myocyte enhancer factor-2A (MEF 2A) has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear. In the present study we aim to assess the role of MEF 2A in the progression of pre-existing atherosclerosis.

Methods: Eighty apolipoprotein E-deficient mice (APOE KO) were randomly allocated to control, scramble and MEF 2A RNA interference (RNAi) groups, and constrictive collars were used to induce plaque formation. Six weeks after surgery, lentiviral shRNA construct was used to silence the expression of MEF 2A. Carotid plaques were harvested for analysis 4 weeks after viral vector transduction. Inflammatory gene expression in the plasma and carotid plaques was determined by using ELISAs and real-time RT-PCR.

Results: The expression level of MEF 2A was significantly reduced in plasma and plaque in the RNAi group, compared to the control and NC groups, whereas the expression level of pro-inflammatory cytokines was markedly increased. Silencing MEF 2A using lentiviral shRNA significantly reduced the plaque collagen content and fibrous cap thickness, as well as increased plaque area. However, silencing MEF 2A had no obvious effect on plaque lipid content.

Conclusions: Lentivirus-mediated MEF 2A shRNA accelerates inflammation and atherosclerosis in APOE KO mice, but has no effect on lipoprotein levels in plasma.

No MeSH data available.


Related in: MedlinePlus