Lentivirus-mediated mouse metalloproteinase meprin α induces formation of atherosclerotic plaques in ApoE-/- mice
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Lentivirus-mediated mouse metalloproteinase meprin α induces formation of atherosclerotic plaques in ApoE-/- mice
Journal of Army Medical UniversityVol. 35, Issue 21, Pages: 2310-2313(2013)
作者机构:
第三军医大学西南医院老年病科
作者简介:
基金信息:
DOI:
CLC:R345;R543.12;R392.3
Published:2013,
Published Online:15 November 2013,
稿件说明:
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HAO PAN, SI LIANGYI, WANG XIAOMEI. Lentivirus-mediated mouse metalloproteinase meprin α induces formation of atherosclerotic plaques in ApoE-/- mice. [J]. Journal of army medical university, 2013, 35(21): 2310-2313.
DOI:
HAO PAN, SI LIANGYI, WANG XIAOMEI. Lentivirus-mediated mouse metalloproteinase meprin α induces formation of atherosclerotic plaques in ApoE-/- mice. [J]. Journal of army medical university, 2013, 35(21): 2310-2313.DOI:
Lentivirus-mediated mouse metalloproteinase meprin α induces formation of atherosclerotic plaques in ApoE-/- mice
Objective To determine the effect of lentivirus-mediated mouse meprin α on the formation of atherosclerotic plaques. Methods Eighteen ApoE
-/-
mice (age 18 mo
nths) were divided randomly into 3 groups
control
LvMep1A
and LvGFP groups. All the mice were fed with high-fat dieting for 14 weeks
and then tail injection with placebo
LvMep1A
or LvGFP respectively at the beginning of the 11th week. Value of weight
blood pressure
and plasma lipid levels were measured by automatic biochemical analyzer. Meprin α protein levels were measured by Western blotting and ELISA respectively. The size of plaque area were determined by HE staining and quantified with Image plus pro software. Apoptotic cell were determined by TUNEL. The inflammatory factors were measured by ELISA. Results Compared with control group
the protein expression of meprin α was significantly increased by 3.7-folds and 3.4-folds in the plasma and vascular tissue respectively (
P
<
0.05). Compared with control group
the body weight and plasma levels of triglycerides
and LDL were significantly increased in LvMep1A mice (
P
<
0.05). On the contrary
the value of HDL level was significantly decreased in LvMep1A mice (
P
<
0.05). Compared with control group
the size of plaque area was significantly increased (
P
<
0.05)
and the percentage of TUNEL positive cells were significantly increased by 58.25% in LvMep1A mice (
P
<
0.05). Additionally
the plasma levels of IL-1β
TNF-α and MMP-9 were significantly increased in LvMep1A mice when compared with control mice (
P
<
0.05). However
the levels of MCP-1 and IL-6 had no significant change in LvMep1A mice (
P
>0.05). Compared with control mice
the values in LvGFP mice have no significant change (
P
>0.05). Conclusion Meprin α significantly induces the formation and progression of atherosclerosis plaque
which might be due to its improving the release of inflammatory factors and inducing cell apoptosis in atherosclerosis plaque.