Effects of Human Full-length Amelogenin and C-terminal Amelogenin Peptide on the Proliferation of Human Mesenchymal Stem Cells Derived from Adipose Tissue
Effects of Human Full-length Amelogenin and C-terminal Amelogenin Peptide on the Proliferation of Human Mesenchymal Stem Cells Derived from Adipose Tissue
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DOI：
10.2174/1381612824666180816093227
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发表时间：
2018-01-01
影响因子：
3.1
通讯作者：
Tanimoto, Kotaro
中科院分区：
文献类型：
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作者：
Ando, Kazuyo;Kunimatsu, Ryo;Tanimoto, Kotaro
成釉原蛋白是釉质基质蛋白，在釉质形成中起着至关重要的作用。以往的研究表明，淀粉原蛋白和淀粉原蛋白c端肽具有细胞信号功能。最近，脂肪细胞来源的间充质干细胞（ADSCs）作为一种潜在的干细胞来源在再生治疗中得到了关注。在本研究中，我们检测了人全长淀粉原蛋白（rh174）和淀粉原蛋白c端肽（amgCP）对ADSCs增殖的影响。在amgCP或rh174存在下培养ADSCs。采用BrdU免疫法和MTS法分析细胞增殖情况。ELISA法检测细胞迁移情况。采用phospho-p44/42 MAPK （Thr202/Tyr204）夹心ELISA和western blotting检测MAPK- erk通路。一种特异性的MAPK抑制剂U0126被用来阻断ERK活性。与未处理的对照细胞相比，rh174和amgCP显著提高了ADSC的增殖和迁移能力（P < 0.05）。2 μ g/ml U0126的存在显著抑制了rh174和amgCP诱导的ADSCs增殖（P < 0.05）。与未处理的ADSCs相比，rh174或amgCP处理后，pERK/tERK比值显著（P < 0.05）升高，而U0126显著抑制了这一升高（P < 0.05）。western blot分析结果相似。总之，amgCP和rh174通过MAPK-ERK信号通路促进ADSC的增殖，ADSC可能对口腔颌面部组织再生有用。
Amelogenins are enamel matrix proteins that play crucial roles in enamel formation. Previous studies have indicated that amelogenin and amelogenin C-terminal peptides have cell-signaling functions. Recently, adipocyte-derived mesenchymal stem cells (ADSCs) have received attention as a potential source of stem cells for use in regeneration therapy. In this study, we examined the effects of human full-length amelogenin (rh174) and amelogenin C-terminal peptide (amgCP) on the proliferation of ADSCs. ADSCs were cultured in the presence of amgCP or rh174. Cell proliferation was analyzed using BrdU immunoassay and MTS assay. Cell migration was evaluated by ELISA. The MAPK-ERK pathway was examined by phospho-p44/42 MAPK (Thr202/Tyr204) sandwich ELISA and western blotting. A specific MAPK inhibitor, U0126, was used to block ERK activity. ADSC proliferation and migration were significantly (P < 0.05) increased in the presence of rh174 or amgCP compared to non-treated control cells. The increased proliferation of ADSCs induced by rh174 or amgCP was significantly (P < 0.05) inhibited in the presence of 2 mu g/ml U0126. The pERK/tERK ratio was significantly (P < 0.05) increased upon treatment with rh174 or amgCP compared to non-treated ADSCs, while this increase was significantly (P < 0.05) suppressed by the addition of U0126. Similar results were found by western blot analysis. In conclusion, amgCP and rh174 increase ADSC proliferation via the MAPK-ERK signaling pathway, and ADSCs may be useful for tissue regeneration in the orofacial region.