کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5528573 1548001 2017 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hyaluronic acid-laminin hydrogels increase neural stem cell transplant retention and migratory response to SDF-1α
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Hyaluronic acid-laminin hydrogels increase neural stem cell transplant retention and migratory response to SDF-1α
چکیده انگلیسی


- A hyaluronicacid-laminin (HA-Lm) hydrogel was shown to promote neural progenitor/stem cell (NPSC) response to SDF-1α in vivo
- The HA-Lm gel significantly increased NPSC transplant retention and migratory response to SDF-1α out to 3 days
- Inhibiting SDF-1α-CXCR4 signaling significantly reduced NPSC migration, but not retention, when transplanted in the HA-Lm gel

The chemokine SDF-1α plays a critical role in mediating stem cell response to injury and disease and has specifically been shown to mobilize neural progenitor/stem cells (NPSCs) towards sites of neural injury. Current neural transplant paradigms within the brain suffer from low rates of retention and engraftment after injury. Therefore, increasing transplant sensitivity to injury-induced SDF-1α represents a method for increasing neural transplant efficacy. Previously, we have reported on a hyaluronic acid-laminin based hydrogel (HA-Lm gel) that increases NPSC expression of SDF-1α receptor, CXCR4, and subsequently, NPSC chemotactic migration towards a source of SDF-1α in vitro. The study presented here investigates the capacity of the HA-Lm gel to promote NPSC response to exogenous SDF-1α in vivo. We observed the HA-Lm gel to significantly increase NPSC transplant retention and migration in response to SDF-1α in a manner critically dependent on signaling via the SDF-1α-CXCR4 axis. This work lays the foundation for development of a more effective cell therapy for neural injury, but also has broader implications in the fields of tissue engineering and regenerative medicine given the essential roles of SDF-1α across injury and disease states.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Matrix Biology - Volumes 60–61, July 2017, Pages 206-216
نویسندگان
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