The effect of incorporation of SDF-1alpha into PLGA scaffolds on stem cell recruitment and the inflammatory response.
The effect of incorporation of SDF-1alpha into PLGA scaffolds on stem cell recruitment and the inflammatory response.
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DOI:
10.1016/j.biomaterials.2010.01.144
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发表时间:
2010-05
期刊:
影响因子:
14
通讯作者:
Tang, Liping
中科院分区:
文献类型:
--
作者:
Thevenot, Paul T.;Nair, Ashwin M.;Shen, Jinhui;Lotfi, Parisa;Ko, Cheng-Yu;Tang, Liping
Despite significant advances in the understanding of tissue responses to biomaterials, most implants are still plagued by inflammatory responses which can lead to fibrotic encapsulation. This is of dire consequence in tissue engineering, where seeded cells and bioactive components are separated from the native tissue, limiting the regenerative potential of the design. Additionally, these interactions prevent desired tissue integration and angiogenesis, preventing functionality of the design. Recent evidence supports that mesenchymal stem cells (MSC) and hematopoietic stem cells (HSC) can have beneficial effects which alter the inflammatory responses and improve healing. The purpose of this study was to examine whether stem cells could be targeted to the site of biomaterial implantation and whether increasing local stem cell responses could improve the tissue response to PLGA scaffold implants. Through incorporation of SDF-1α through factor adsorption and mini-osmotic pump delivery, the host-derived stem cell response can be improved resulting in 3X increase in stem cell populations at the interface for up to 2 weeks. These interactions were found to significantly alter the acute mast cell responses, reducing the number of mast cells and degranulated mast cells near the scaffold implants. This led to subsequent downstream reduction in the inflammatory cell responses, and through altered mast cell activation and stem cell participation, increased angiogenesis and decreased fibrotic responses to the scaffold implants. These results support that enhanced recruitment of autologous stem cells can improve the tissue responses to biomaterial implants through modifying/bypassing inflammatory cell responses and jumpstarting stem cell participation in healing at the implant interface.
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DOI:
10.4049/jimmunol.0900803
发表时间:
2009-07-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Fiorina P;Jurewicz M;Augello A;Vergani A;Dada S;La Rosa S;Selig M;Godwin J;Law K;Placidi C;Smith RN;Capella C;Rodig S;Adra CN;Atkinson M;Sayegh MH;Abdi R
通讯作者:
Abdi R
影响因子:
4.4
作者:
El-Shazly, A;Berger, P;Tunon-de-Lara, JM
通讯作者:
Tunon-de-Lara, JM
影响因子:
5.2
作者:
Copland, Ian B.;Lord-Dufour, Simon;Galipeau, Jacques
通讯作者:
Galipeau, Jacques
影响因子:
20.3
作者:
Hattori, K;Heissig, B;Moore, MAS
通讯作者:
Moore, MAS
影响因子:
14
作者:
Hosseinkhani, Hossein;Hosseinkhani, Mohsen;Tabata, Yasuhiko
通讯作者:
Tabata, Yasuhiko