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

Carotid plaques in the control, NC and MEF 2A RNAi groups.Cross-sections of plaques in the control, NC and RNAi groups were stained with HE, ORO and masson’s trichrome. magnification 200×.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0121823.g005: Carotid plaques in the control, NC and MEF 2A RNAi groups.Cross-sections of plaques in the control, NC and RNAi groups were stained with HE, ORO and masson’s trichrome. magnification 200×.

Mentions: The plaque area in cross-section from the MEF 2A shRNA group is 58.7 ± 8.4 × 103 μm2, which was statistical higher than the control and NC groups(42.3 ± 6.5 × 103 μm2 and 43.7 ± 7.1 × 103 μm2; P < 0.01, Fig. 4D). Fibrous cap thickness was significant lower in the MEF 2A shRNA group (8.63 ± 0.92μm) than that in the control and NC groups (12.89 ± 1.75 and 13.29 ± 1.55 μm; P < 0.01, Fig. 4E). As expected, no obvious differences in plaque area and fibrous cap thickness were found between the scramble control and NC groups (Figs. 4D-G and 5).


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)

Carotid plaques in the control, NC and MEF 2A RNAi groups.Cross-sections of plaques in the control, NC and RNAi groups were stained with HE, ORO and masson’s trichrome. magnification 200×.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0121823.g005: Carotid plaques in the control, NC and MEF 2A RNAi groups.Cross-sections of plaques in the control, NC and RNAi groups were stained with HE, ORO and masson’s trichrome. magnification 200×.
Mentions: The plaque area in cross-section from the MEF 2A shRNA group is 58.7 ± 8.4 × 103 μm2, which was statistical higher than the control and NC groups(42.3 ± 6.5 × 103 μm2 and 43.7 ± 7.1 × 103 μm2; P < 0.01, Fig. 4D). Fibrous cap thickness was significant lower in the MEF 2A shRNA group (8.63 ± 0.92μm) than that in the control and NC groups (12.89 ± 1.75 and 13.29 ± 1.55 μm; P < 0.01, Fig. 4E). As expected, no obvious differences in plaque area and fibrous cap thickness were found between the scramble control and NC groups (Figs. 4D-G and 5).

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