4.8 Article

Ferrimagnetic Nanochains-Based Mesenchymal Stem Cell Engineering for Highly Efficient Post-Stroke Recovery

期刊

ADVANCED FUNCTIONAL MATERIALS
卷 29, 期 24, 页码 -

出版社

WILEY-V C H VERLAG GMBH
DOI: 10.1002/adfm.201900603

关键词

ferrimagnetic iron oxide nanochains; genetic engineering; ischemic cerebrum homing; mesenchymal stem cells; post-stroke recovery

资金

  1. National Key Research and Development Program of China [2016YFA0203600]
  2. National Natural Science Foundation of China [31822019, 81620108028, 81703423, 91859116, 51703195, 81473143]
  3. One Belt and One Road International Cooperation Project from Key Research and Development Program of Zhejiang Province [2019C04024]
  4. China Postdoctoral Science Foundation [2018M640568, 2016M601938]
  5. Fundamental Research Funds for the Central Universities [2018QNA7021, 2018QNA7020]
  6. Zhejiang Provincial Natural Science Foundation of China [LGF19C100002]
  7. Thousand Talents Program for Distinguished Young Scholars
  8. Research Center Program of Institute for Basic Science in Korea [IBS-R006-D1]
  9. National Research Foundation of Korea [IBS-R006-D1-2019-A00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Unsatisfactory post-stroke recovery has long been a negative factor in the prognosis of ischemic stroke due to the lack of pharmacological treatments. Mesenchymal stem cells (MSCs)-based therapy has recently emerged as a promising strategy redefining stroke treatment; however, its effectiveness has been largely restricted by insufficient therapeutic gene expression and inadequate cell numbers in the ischemic cerebrum. Herein, a non-viral and magnetic field-independent gene transfection approach is reported, using magnetosome-like ferrimagnetic iron oxide nanochains (MFIONs), to genetically engineer MSCs for highly efficient post-stroke recovery. The 1D MFIONs show efficient cellular uptake by MSCs, which results in highly efficient genetic engineering of MSCs to overexpress brain-derived neurotrophic factor for treating ischemic cerebrum. Moreover, the internalized MFIONs promote the homing of MSCs to the ischemic cerebrum by upregulating CXCR4. Consequently, a pronounced recovery from ischemic stroke is achieved using MFION-engineered MSCs in a mouse model.

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