Platelet-rich plasma enhances the proliferation of human adipose stem cells through multiple signaling pathways.
Platelet-rich plasma enhances the proliferation of human adipose stem cells through multiple signaling pathways.
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DOI：
10.1186/s13287-018-0851-z
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发表时间：
2018-04-16
影响因子：
7.5
通讯作者：
Kusumoto K
中科院分区：
文献类型：
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作者：
Lai F;Kakudo N;Morimoto N;Taketani S;Hara T;Ogawa T;Kusumoto K
富血小板血浆（PRP）是一种自体血液产品，含有高浓度的几种生长因子。血小板源性生长因子（PDGF）-BB是人脂肪源性干细胞（hASCs）的潜在有丝分裂原。PRP刺激hASCs的增殖;然而，PRP激活的信号通路仍不清楚。用或不用PRP或PDGF-BB培养hASC，并评估增殖。hASC也用PRP或PDGF-BB处理，有或没有伊马替尼，其是PDGF受体酪氨酸激酶抑制剂，或索拉非尼，其是多激酶抑制剂。使用抗PDGF抗体（Abcam，剑桥，UK）通过细胞计数检查细胞增殖的抑制。我们评估了各种蛋白激酶如ERK 1/2、JNK、p38和Akt的抑制剂对hASCs增殖的影响。在用1%PRP或10 ng/ml PDGF-BB处理的细胞中，增殖显著促进，并且伊马替尼和索拉非尼都抑制这种增殖。抗PDGF抗体（0.5和2 μg/ml）显著抑制hASCs的增殖。PRP介导的hASC增殖被ERK 1/2、Akt和JNK抑制剂阻断，但不被p38抑制剂阻断。PRP促进hASC增殖，PRP中的PDGF-BB在诱导hASC增殖中起主要作用。PRP通过ERK 1/2、PI 3 K/Akt和JNK信号通路促进hASC增殖。
Platelet-rich plasma (PRP) is an autologous blood product that contains a high concentration of several growth factors. Platelet-derived growth factor (PDGF)-BB is a potential mitogen for human adipose-derived stem cells (hASCs). PRP stimulates proliferation of hASCs; however, the signaling pathways activated by PRP remain unclear. hASCs were cultured with or without PRP or PDGF-BB, and proliferation was assessed. hASCs were also treated with PRP or PDGF-BB with or without imatinib, which is a PDGF receptor tyrosine kinase inhibitor, or sorafenib, which is a multikinase inhibitor. Inhibition of cell proliferation was examined using anti-PDGF antibody (Abcam, Cambridge, UK), by cell counting. We assessed the effects of inhibitors of various protein kinases such as ERK1/2, JNK, p38, and Akt on the proliferation of hASCs. The proliferation was remarkably promoted in cells treated with either 1% PRP or 10 ng/ml PDGF-BB, and both imatinib and sorafenib inhibited this proliferation. Anti-PDGF antibody (0.5 and 2 μg/ml) significantly decreased the proliferation of hASCs compared with control. PRP-mediated hASC proliferation was blocked by inhibitors of ERK1/2, Akt, and JNK, but not by an inhibitor of p38. PRP promotes hASC proliferation, and PDGF-BB in PRP plays a major role in inducing the proliferation of hASCs. PRP promotes hASC proliferation via ERK1/2, PI3K/Akt, and JNK signaling pathways.