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天冬氨酸对紫外线A诱导的人脂肪组织来源间充质干细胞干性下调的拮抗作用

Antagonizing Effects of Aspartic Acid against Ultraviolet A-Induced Downregulation of the Stemness of Human Adipose Tissue-Derived Mesenchymal Stem Cells.

作者信息

Jung Kwangseon, Cho Jae Youl, Soh Young-Jin, Lee Jienny, Shin Seoung Woo, Jang Sunghee, Jung Eunsun, Kim Min Hee, Lee Jongsung

机构信息

Department of Convergence Biomedical Science & Engineering, Eulji University, Seongnam City, Gyunggi Do, Republic of Korea; Skincure Life Science Institute, Seongnam City, Gyunggi Do, Republic of Korea.

Department of Genetic Engineering, Sungkyunkwan University, Suwon-Si, Gyeonggi-Do, Republic of Korea.

出版信息

PLoS One. 2015 Apr 24;10(4):e0124417. doi: 10.1371/journal.pone.0124417. eCollection 2015.

DOI:10.1371/journal.pone.0124417
PMID:25909857
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4409053/
Abstract

Ultraviolet A (UVA) irradiation is responsible for a variety of changes in cell biology. The purpose of this study was to investigate effects of aspartic acid on UVA irradiation-induced damages in the stemness properties of human adipose tissue-derived mesenchymal stem cells (hAMSCs). Furthermore, we elucidated the UVA-antagonizing mechanisms of aspartic acid. The results of this study showed that aspartic acid attenuated the UVA-induced reduction of the proliferative potential and stemness of hAMSCs, as evidenced by increased proliferative activity in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and upregulation of stemness-related genes OCT4, NANOG, and SOX2 in response to the aspartic acid treatment. UVA-induced reduction in the mRNA level of hypoxia-inducible factor (HIF)-1α was also significantly recovered by aspartic acid. In addition, the antagonizing effects of aspartic acid against the UVA effects were found to be mediated by reduced production of PGE2 through the inhibition of JNK and p42/44 MAPK. Taken together, these findings show that aspartic acid improves reduced stemness of hAMSCs induced by UVA and its effects are mediated by upregulation of HIF-1α via the inhibition of PGE2-cAMP signaling. In addition, aspartic acid may be used as an antagonizing agent to mitigate the effects of UVA.

摘要

紫外线A（UVA）照射会导致细胞生物学发生多种变化。本研究的目的是探讨天冬氨酸对UVA照射诱导的人脂肪组织来源间充质干细胞（hAMSCs）干性特性损伤的影响。此外，我们阐明了天冬氨酸拮抗UVA的机制。本研究结果表明，天冬氨酸减弱了UVA诱导的hAMSCs增殖潜能和干性的降低，3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐（MTT）试验中增殖活性的增加以及天冬氨酸处理后干性相关基因OCT4、NANOG和SOX2的上调证明了这一点。天冬氨酸还显著恢复了UVA诱导的缺氧诱导因子（HIF）-1α mRNA水平的降低。此外，发现天冬氨酸对UVA效应的拮抗作用是通过抑制JNK和p42/44 MAPK减少PGE2的产生来介导的。综上所述，这些发现表明天冬氨酸改善了UVA诱导的hAMSCs干性降低，其作用是通过抑制PGE2-cAMP信号上调HIF-1α介导的。此外，天冬氨酸可用作拮抗药物以减轻UVA的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/25decc805144/pone.0124417.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/2938adb221fb/pone.0124417.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/d3e033673714/pone.0124417.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/acd5a8d2fc23/pone.0124417.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/d1882cf9a5d5/pone.0124417.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/f57e10fb065b/pone.0124417.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/75749c6120e8/pone.0124417.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/25decc805144/pone.0124417.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/2938adb221fb/pone.0124417.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/d3e033673714/pone.0124417.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/acd5a8d2fc23/pone.0124417.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/d1882cf9a5d5/pone.0124417.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/f57e10fb065b/pone.0124417.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/75749c6120e8/pone.0124417.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2484/4409053/25decc805144/pone.0124417.g007.jpg

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