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雌激素受体并不影响心肌梗死后的血管生成。

Estrogen receptors do not influence angiogenesis after myocardial infarction.

机构信息

Department of Cardiology, Karolinska Institute, Clinical Research Center, Stockholm, Sweden.

出版信息

Scand Cardiovasc J. 2011 Aug;45(4):215-22. doi: 10.3109/14017431.2011.569941. Epub 2011 Apr 12.

Abstract

BACKGROUND

There is controversy on whether estrogen receptors are present and functioning in the myocardium. Aims. To explore if after myocardial infarction (MI) estrogen receptors α (ERα) and β (ERβ) are upregulated in myocardial tissue and to explore if the presence/ absence of ERα or ERβ influences angiogenesis after MI.

METHODS

MI was induced by ligation of the left anterior descending artery in knockout (KO) mice, ERαKO and ERβKO, respectively, and non-KO littermate-controls, C57Bl/6 mice. The hearts were harvested after 12 days. A part of the periinfarct tissue was collected for ERα and ERβ mRNA expression determination by real-time polymerase chain reaction. Using immunohistochemistry, ERα and ERβ protein expression and capillary and arteriolar densities were blindly determined in the periinfarct area.

RESULTS

In myocardium disrupted mRNA was upregulated in both ERαKO and ERβKO, (p < 0.005) and did not change after MI. There was no change in mRNA expression of ERα or ERβ in wild type mice after MI. Expression of ERβ in ERαKO and of ERα in ERβKO did not change. Following MI ERα or ERβ could not be demonstrated by immunohistochemistry in either wild type or ERαKO or ERβKO. The capillary and arteriolar densities after MI did not differ between the groups in the periinfarct area.

CONCLUSIONS

Although disrupted ER mRNA is upregulated in myocardium of ER knockout mice, no change in these or native receptors occurs following MI. At least in this model ER therefore seems not to have a role in myocardial arteriogenesis and angiogenesis after MI.

摘要

背景

关于雌激素受体是否存在于心肌中并发挥作用存在争议。目的:探讨心肌梗死后(MI)雌激素受体α(ERα)和β(ERβ)是否在心肌组织中上调,并探讨 ERα 或 ERβ 的存在/缺失是否影响 MI 后的血管生成。

方法

通过结扎左前降支在敲除(KO)小鼠、ERαKO 和 ERβKO 以及非 KO 同窝对照 C57Bl/6 小鼠中诱导 MI。12 天后收获心脏。采集梗死周围组织的一部分,通过实时聚合酶链反应测定 ERα 和 ERβ mRNA 的表达。使用免疫组织化学法,在梗死周围区域盲法测定 ERα 和 ERβ 蛋白表达和毛细血管及小动脉密度。

结果

在心肌中断的 mRNA 在 ERαKO 和 ERβKO 中均上调(p<0.005),MI 后没有变化。MI 后野生型小鼠 ERα 或 ERβ 的 mRNA 表达没有变化。在 ERαKO 中 ERβ 的表达和在 ERβKO 中 ERα 的表达没有改变。MI 后,无论是在野生型还是 ERαKO 或 ERβKO 中,都无法通过免疫组织化学检测到 ERα 或 ERβ。MI 后梗死周围区域各组毛细血管和小动脉密度无差异。

结论

尽管 ER 敲除小鼠心肌中断的 ER mRNA 上调,但 MI 后这些或天然受体没有变化。至少在这种模型中,ER 似乎在 MI 后心肌血管生成和血管生成中没有作用。

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