Platelets‐rich plasma (PRP) can produce growth factors (GFs) to improve angiogenesis. However, direct injection of PRP does not lead to highly localized GFs. The current study employs a mussel‐inspired polydopamine to immobilize PRP on gelatin microspheres (GMs) with the purpose of bridging adipose micro‐tissues to help implanted fat survive (GM‐pDA‐PRP). Enhanced PRP adhesion leads to a prolonged and localized production of GFs, which is verified by platelet counting and by ELISA of vascular endothelial growth factors (VEGFs) and of platelet derived growth factors (PDGFs). The GM‐pDA‐PRP “hatches” a microenvironment for the proliferation of adipose‐derived stem cells. After the adipose micro‐tissue has bridged with GM‐pDA‐PRP after 16 weeks, triple‐fluorescence staining reveals that the mature adipocytes, blood vessels, and capillaries are arranged like in normal adipose tissue. The survival fat increases significantly compared to that in control, PRP, and GM‐PRP groups (84.8 ± 11.4% versus 47.8 ± 8.9%, 56.9 ± 9.7%, and 60.2 ± 10.5%, respectively). Both histological assessments and CD31 immunofluorescence indicate that the improvement of angiogenesis in GM‐pDA‐PRP is higher than in the fat graft group (6.4‐fold in quantitative CD31 positive cells). The CD34 positive cells in the GM‐pDA‐PRP group are around 3.5‐fold the amount in the fat graft group, which suggests that more stem cells migrate to the implant area. Cell proliferation staining shows that the number of Ki67 positive cells is around five times as high as that in the fat graft group.

中文翻译：

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贻贝激发的可注射血小板的血浆在微球上的固定化脂肪微组织，通过控制PDGF和VEGF的释放，血管生成，干细胞迁移来改善自体脂肪移植

富含血小板的血浆（PRP）可以产生生长因子（GFs）以改善血管生成。但是，直接注射PRP不会导致高度局部化的GF。本研究采用贻贝启发性的聚多巴胺将PRP固定在明胶微球（GMs）上，目的是桥接脂肪微组织以帮助植入的脂肪存活（GM-pDA-PRP）。增强的PRP附着力会导致GFs的长期和局部产生，这可以通过血小板计数和ELISA验证，血管内皮生长因子（VEGF）和血小板衍生的生长因子（PDGFs）。GM-pDA-PRP“孵化”了脂肪干细胞增殖的微环境。16周后，脂肪微组织与GM-pDA-PRP桥接后，三重荧光染色显示成熟的脂肪细胞，血管，毛细血管的排列就像正常的脂肪组织一样。与对照组，PRP和GM-PRP组相比，存活脂肪显着增加（分别为84.8±11.4％和47.8±8.9％，56.9±9.7％和60.2±10.5％）。组织学评估和CD31免疫荧光均表明，GM‐pDA‐PRP中血管生成的改善高于脂肪移植组（定量CD31阳性细胞中的6.4倍）。GM‐pDA‐PRP组的CD34阳性细胞约为脂肪移植组的3.5倍，这表明更多的干细胞迁移至植入区域。细胞增殖染色显示，Ki67阳性细胞数量约为脂肪移植组的五倍。和GM-PRP组（分别为84.8±11.4％和47.8±8.9％，56.9±9.7％和60.2±10.5％）。组织学评估和CD31免疫荧光均表明，GM‐pDA‐PRP中血管生成的改善高于脂肪移植组（定量CD31阳性细胞中的6.4倍）。GM‐pDA‐PRP组的CD34阳性细胞约为脂肪移植组的3.5倍，这表明更多的干细胞迁移至植入区域。细胞增殖染色显示，Ki67阳性细胞数量约为脂肪移植组的五倍。和GM-PRP组（分别为84.8±11.4％和47.8±8.9％，56.9±9.7％和60.2±10.5％）。组织学评估和CD31免疫荧光均表明，GM‐pDA‐PRP中血管生成的改善高于脂肪移植组（定量CD31阳性细胞中的6.4倍）。GM‐pDA‐PRP组的CD34阳性细胞约为脂肪移植组的3.5倍，这表明更多的干细胞迁移至植入区域。细胞增殖染色显示，Ki67阳性细胞数量约为脂肪移植组的五倍。定量CD31阳性细胞的4倍）。GM‐pDA‐PRP组的CD34阳性细胞约为脂肪移植组的3.5倍，这表明更多的干细胞迁移至植入区域。细胞增殖染色显示，Ki67阳性细胞数量约为脂肪移植组的五倍。定量CD31阳性细胞的4倍）。GM‐pDA‐PRP组的CD34阳性细胞约为脂肪移植组的3.5倍，这表明更多的干细胞迁移至植入区域。细胞增殖染色显示，Ki67阳性细胞数量约为脂肪移植组的五倍。