Mesenchymal stem cells and extracellular matrix scaffold promote muscle regeneration by synergistically regulating macrophage polarization toward the M2 phenotype.
Mesenchymal stem cells and extracellular matrix scaffold promote muscle regeneration by synergistically regulating macrophage polarization toward the M2 phenotype.
复制标题
间充质干细胞和细胞外基质支架通过协同调节巨噬细胞极化向 M2 表型促进肌肉再生
DOI:
10.1186/s13287-018-0821-5
复制
发表时间:
2018-04-03
影响因子:
7.5
通讯作者:
Jin Y
中科院分区:
文献类型:
--
作者:
Qiu X;Liu S;Zhang H;Zhu B;Su Y;Zheng C;Tian R;Wang M;Kuang H;Zhao X;Jin Y
Skeletal muscle plays an important role in the body’s physiology but there are still no effective treatments for volumetric muscle loss (VML) resulting from severe traumatic injury or tumor excision. Recent studies show that a tissue engineering strategy using a compound containing mesenchymal stem cells (MSCs) and decellularized extracellular matrix (ECM) scaffold generates significant regenerative effects on VML injury, but the underlying mechanisms are not fully understood. The characteristics of human umbilical cord MSCs, including multiplication capacity and multidifferentiation ability, were determined. We constructed a compound containing MSCs and decellularized ECM scaffold which was used for tissue regeneration in a VML model. We found that MSCs and decellularized ECM scaffold generated synergistic effects on promoting skeletal muscle tissue regeneration. Interestingly, both MSCs and decellularized ECM scaffold could promote macrophage polarization toward the M2 phenotype and suppress macrophage polarization toward the M1 phenotype, which is widely regarded as an important promoting factor in tissue regeneration. More importantly, MSCs and decellularized ECM scaffold generate synergistic promoting effects on macrophage polarization toward the M2 phenotype, not just an additive effect. Our findings uncover a previously unknown mechanism that MSCs and decellularized ECM scaffold promote tissue regeneration via collaboratively regulating macrophage polarization. The online version of this article (10.1186/s13287-018-0821-5) contains supplementary material, which is available to authorized users.
登录
查看更多内容
影响因子:
3.8
作者:
Duffy RM;Sun Y;Feinberg AW
通讯作者:
Feinberg AW
影响因子:
14
作者:
Ham, Onju;Song, Byeong-Wook;Hwang, Ki-Chul
通讯作者:
Hwang, Ki-Chul
影响因子:
--
作者:
De Coppi, Paolo;Bellini, Silvia;Paolo Parnigotto, Pier
通讯作者:
Paolo Parnigotto, Pier
DOI:
10.5435/00124635-201102001-00007
发表时间:
2011-01-01
影响因子:
3.2
作者:
Grogan, Brian F.;Hsu, Joseph R.
通讯作者:
Hsu, Joseph R.
影响因子:
2.6
作者:
Fuoco C;Petrilli LL;Cannata S;Gargioli C
通讯作者:
Gargioli C