PRP會促進脂肪幹細胞的增生修復
PRP會促進脂肪幹細胞的增生修復
研究進行在有或沒有PRP或PDGF-BB的情況下培養hASCs，並評估增殖情況，結果用1% PRP或10 ng/ml PDGF-BB處理後的細胞增殖顯著促進，並且imatinib和sorafenib都抑制了這種增殖。所以PRP會促進hASCs增殖，其主要作用成分是PRP中的PDGF-BB。PRP會藉由ERK1/2、PI3K/Akt 和 JNK訊息傳遞促進 hASC 增殖。
PRP科技新知- PRP會促進脂肪幹細胞的增生修復
研究背景：
PRP是一種血液製品，含有高濃度的多種生長因子。血小板衍生生長因子 (PDGF)-BB是人類脂肪幹細胞(hASCs)的潛在有絲分裂原。PRP可刺激 hASCs的增殖；然而，PRP激活的訊息傳遞路徑仍不清楚。
研究方法：
在有或沒有PRP或PDGF-BB的情況下培養hASCs，並評估增殖情況。 除上述有或無PRP 或 PDGF-BB外，也在hASCs加或不加imatinib（Glivec基利克，這是一種 PDGF標靶抑制劑，常用於急性淋巴性白血病的治療）或sorafenib （Nexavar蕾莎瓦，這是另一種多功能標靶抑制劑，常用於肝癌與甲狀腺癌的治療）。使用抗PDGF抗體（Abcam，Cambridge，UK）通過細胞計數器來檢查細胞增殖的狀況，並評估各種蛋白激酶抑製劑如 ERK1/2、JNK、p38 和 Akt 對 hASCs增殖的影響。
結果：
用1% PRP或10 ng/ml PDGF-BB處理後的細胞增殖顯著促進，並且imatinib和sorafenib都抑制了這種增殖。與對照組相比，抗PDGF抗體（0.5和2 mug/ml）顯著降低了hASC的增殖。PRP所誘導的hASC增殖會被 ERK1/2、Akt 和 JNK 抑製劑所阻斷，但不會被 p38 抑製劑阻斷。
結論：
PRP會促進hASCs增殖，其主要作用成分是PRP中的PDGF-BB。PRP會藉由ERK1/2、PI3K/Akt 和 JNK訊息傳遞促進 hASC 增殖。
[此文章提供了PRP促進脂肪幹細胞的增生修復的理論基礎]
原文摘要:
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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 mug/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.
CONCLUSIONS: 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.
文章出處:
Lai F, Kakudo N, Morimoto N, Taketani S, Hara T, Ogawa T, Kusumoto K: Platelet-rich plasma enhances the proliferation of human adipose stem cells through multiple signaling pathways. Stem Cell Res Ther 2018, 9(1):107.
研究背景：
PRP是一種血液製品，含有高濃度的多種生長因子。血小板衍生生長因子 (PDGF)-BB是人類脂肪幹細胞(hASCs)的潛在有絲分裂原。PRP可刺激 hASCs的增殖；然而，PRP激活的訊息傳遞路徑仍不清楚。
研究方法：
在有或沒有PRP或PDGF-BB的情況下培養hASCs，並評估增殖情況。 除上述有或無PRP 或 PDGF-BB外，也在hASCs加或不加imatinib（Glivec基利克，這是一種 PDGF標靶抑制劑，常用於急性淋巴性白血病的治療）或sorafenib （Nexavar蕾莎瓦，這是另一種多功能標靶抑制劑，常用於肝癌與甲狀腺癌的治療）。使用抗PDGF抗體（Abcam，Cambridge，UK）通過細胞計數器來檢查細胞增殖的狀況，並評估各種蛋白激酶抑製劑如 ERK1/2、JNK、p38 和 Akt 對 hASCs增殖的影響。
結果：
用1% PRP或10 ng/ml PDGF-BB處理後的細胞增殖顯著促進，並且imatinib和sorafenib都抑制了這種增殖。與對照組相比，抗PDGF抗體（0.5和2 mug/ml）顯著降低了hASC的增殖。PRP所誘導的hASC增殖會被 ERK1/2、Akt 和 JNK 抑製劑所阻斷，但不會被 p38 抑製劑阻斷。
結論：
PRP會促進hASCs增殖，其主要作用成分是PRP中的PDGF-BB。PRP會藉由ERK1/2、PI3K/Akt 和 JNK訊息傳遞促進 hASC 增殖。
[此文章提供了PRP促進脂肪幹細胞的增生修復的理論基礎]
原文摘要:
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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 mug/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.
CONCLUSIONS: 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.
文章出處:
Lai F, Kakudo N, Morimoto N, Taketani S, Hara T, Ogawa T, Kusumoto K: Platelet-rich plasma enhances the proliferation of human adipose stem cells through multiple signaling pathways. Stem Cell Res Ther 2018, 9(1):107.