PDF(Pubmed)
Abstract：
Platelet-rich fibrin (PRF), the coagulated plasma of fractionated blood, is widely used to support tissue regeneration in dentistry, and the underlying cellular and molecular mechanisms are increasingly being understood. Periodontal connective tissues steadily express CXCL8, a chemokine that attracts granulocytes and lymphocytes, supporting homeostatic immunity. Even though PRF is considered to dampen inflammation, it should not be ruled out that PRF increases the expression of CXCL8 in gingival fibroblasts. To test this hypothesis, we conducted a bioassay where gingival fibroblasts were exposed to PRF lysates and the respective serum. We show here that PRF lysates and, to a lesser extent, PRF serum increased the expression of CXCL8 by the gingival fibroblasts, as confirmed by immunoassay. SB203580, the inhibitor of p38 mitogen-activated protein kinase, reduced CXCL8 expression. Consistently, PRF lysates and, to a weaker range, the PRF serum also caused phosphorylation of p38 in gingival fibroblasts. Assuming that PRF is a rich source of growth factors, the TGF-β receptor type I kinase inhibitor SB431542 decreased the PRF-induced expression and translation of CXCL8. The findings suggest that PRF lysates and the respective serum drive CXCL8 expression by activating TGF-β and p38 signaling in gingival fibroblasts.
摘要：
富血小板纤维蛋白(PRF),分馏血液的凝固血浆，广泛用于支持牙科组织再生，以及潜在的细胞和分子机制越来越被理解。牙周结缔组织稳定表达CXCL8，一种吸引粒细胞和淋巴细胞的趋化因子，支持稳态免疫。即使PRF被认为可以抑制炎症，不应排除PRF增加牙龈成纤维细胞中CXCL8的表达。为了检验这个假设，我们进行了一项生物测定，其中牙龈成纤维细胞暴露于PRF裂解物和各自的血清。我们在这里显示PRF裂解物和，在较小程度上，PRF血清增加牙龈成纤维细胞CXCL8的表达，经免疫测定证实。SB203580，p38丝裂原活化蛋白激酶的抑制剂，降低CXCL8表达。始终如一，PRF裂解物和，到一个较弱的范围，PRF血清也引起牙龈成纤维细胞中p38的磷酸化。假设PRF是生长因子的丰富来源，TGF-β受体I型激酶抑制剂SB431542降低了PRF诱导的CXCL8的表达和翻译。研究结果表明，PRF裂解物和各自的血清通过激活牙龈成纤维细胞中的TGF-β和p38信号传导来驱动CXCL8表达。
