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外骨膜蛋白肽刺激大型哺乳动物的心肌再生可改善心肌梗死后的功能，但会增加心肌纤维化。

Stimulating myocardial regeneration with periostin Peptide in large mammals improves function post-myocardial infarction but increases myocardial fibrosis.

机构信息

Cardiovascular Research Center, Department of Cardiology, Mount Sinai School of Medicine, New York, New York, USA.

出版信息

PLoS One. 2013 May 20;8(5):e59656. doi: 10.1371/journal.pone.0059656. Print 2013.

DOI:10.1371/journal.pone.0059656
PMID:23700403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3659021/
Abstract

AIMS

Mammalian myocardium has a finite but limited capacity to regenerate. Experimentally stimulating proliferation of cardiomyocytes with extracellular regeneration factors like periostin enhances cardiac repair in rodents. The aim of this study was to develop a safe method for delivering regeneration factors to the heart and to test the functional and structural effects of periostin peptide treatment in a large animal model of myocardial infarction (MI).

METHODS AND RESULTS

We developed a controlled release system to deliver recombinant periostin peptide into the pericardial space. A single application of this method was performed two days after experimental MI in swine. Animals were randomly assigned to receive either saline or periostin peptide. Experimental groups were compared at baseline, day 2, 1 month and 3 months. Treatment with periostin peptide increased the EF from 31% to 41% and decreased by 22% the infarct size within 12 weeks. Periostin peptide-treated animals had newly formed myocardium strips within the infarct scar, leading to locally improved myocardial function. In addition the capillary density was increased in animals receiving periostin. However, periostin peptide treatment increased myocardial fibrosis in the remote region at one week and 12 weeks post-treatment.

CONCLUSION

Our study shows that myocardial regeneration through targeted peptides is possible. However, in the case of periostin the effects on cardiac fibrosis may limit its clinical application as a viable therapeutic strategy.

摘要

目的

哺乳动物的心肌具有有限但有限的再生能力。实验上，通过外源性再生因子如骨膜蛋白刺激心肌细胞增殖，可增强啮齿动物的心脏修复。本研究的目的是开发一种安全的方法将再生因子递送到心脏，并在心肌梗死（MI）的大动物模型中测试骨膜蛋白肽治疗的功能和结构影响。

方法和结果

我们开发了一种控释系统，将重组骨膜蛋白肽递送到心包腔。在猪实验性 MI 后两天进行单次应用。动物随机分为盐水或骨膜蛋白肽组。在基线、第 2 天、1 个月和 3 个月比较实验组。骨膜蛋白肽治疗将 EF 从 31%提高到 41%，并在 12 周内将梗死面积减少 22%。骨膜蛋白肽治疗的动物在梗死瘢痕内形成了新的心肌带，导致局部心肌功能改善。此外，接受骨膜蛋白肽治疗的动物的毛细血管密度增加。然而，骨膜蛋白肽治疗在治疗后 1 周和 12 周时增加了远程区域的心肌纤维化。

结论

我们的研究表明，通过靶向肽进行心肌再生是可能的。然而，在骨膜蛋白的情况下，对心肌纤维化的影响可能限制其作为可行治疗策略的临床应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/e8afc07132aa/pone.0059656.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/66bf13c18638/pone.0059656.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/01810e50e897/pone.0059656.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/9edd4bd732db/pone.0059656.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/48456f792453/pone.0059656.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/ddc2099ffad4/pone.0059656.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/4535b3c642f9/pone.0059656.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/e17e918b2e8b/pone.0059656.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/e8afc07132aa/pone.0059656.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/66bf13c18638/pone.0059656.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/0b20485ed5fc/pone.0059656.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/01810e50e897/pone.0059656.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/9edd4bd732db/pone.0059656.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/48456f792453/pone.0059656.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/ddc2099ffad4/pone.0059656.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/4535b3c642f9/pone.0059656.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/e17e918b2e8b/pone.0059656.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf50/3659021/e8afc07132aa/pone.0059656.g009.jpg

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