Ying-Hao Han1, Mei-Hua Jin2, Ying-Hua Jin3, Nan-Nan Yu2, Jun Liu2, Yong-Qing Zhang2, Yu-Dong Cui2, Ai-Guo Wang4, Dong-Seok Lee5, Sun-Uk Kim6, Ji-Su Kim7, Taeho Kwon8, Hu-Nan Sun1. 1. College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Heilongjiang, P.R. China hyhbynd@163.com kwon@kribb.re.kr sunhunan76@163.com. 2. College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Heilongjiang, P.R. China. 3. Library and Information Center, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Heilongjiang, P.R. China. 4. Laboratory Animal center, Dalian Medical University, Dalian, P.R. China. 5. School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University, Daegu, Republic of Korea. 6. Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si, Republic of Korea. 7. Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea. 8. Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea hyhbynd@163.com kwon@kribb.re.kr sunhunan76@163.com.
Abstract
BACKGROUND/AIM: Dermal mesenchymal stem cells (DMSCs) are pluripotent stem cells found in the skin which maintain the thickness of the dermal layer and participate in skin wound healing. MATERIALS AND METHODS: The MTT assay was performed to detect cell proliferation and cell-cycle progression and cell-surface markers were assessed by flow cytometry. The levels of proteins in related signaling pathways were detected by western blotting assay and the translocation of β-catenin into the nucleus were detected by immunofluorescence. Red oil O staining was performed to examine the differentiational ability of DMSCs. RESULTS: Knockout of PRDX2 inhibited DMSC cell growth, and cell-cycle arrest at G0/G1 phase; p16, p21 and cyclin D1 expression levels in Prdx2 knockout DMSCs were significantly increased. Furthermore, AKT phosphorylation were significantly increased in Prdx2 knockout DMSCs, GSK3β activity were inhibited, result in β-Catenin accumulated in the nucleus. CONCLUSION: In conclusion, these results demonstrated that PRDX2 plays a pivotal role in regulating the proliferation of DMSCs, and this is closely related to the AKT/glycogen synthase kinase 3 beta/β-catenin signaling pathway. Copyright
BACKGROUND/AIM: Dermal mesenchymal stem cells (DMSCs) are pluripotent stem cells found in the skin which maintain the thickness of the dermal layer and participate in skin wound healing. MATERIALS AND METHODS: The MTT assay was performed to detect cell proliferation and cell-cycle progression and cell-surface markers were assessed by flow cytometry. The levels of proteins in related signaling pathways were detected by western blotting assay and the translocation of β-catenin into the nucleus were detected by immunofluorescence. Red oil O staining was performed to examine the differentiational ability of DMSCs. RESULTS: Knockout of PRDX2 inhibited DMSC cell growth, and cell-cycle arrest at G0/G1 phase; p16, p21 and cyclin D1 expression levels in Prdx2 knockout DMSCs were significantly increased. Furthermore, AKT phosphorylation were significantly increased in Prdx2 knockout DMSCs, GSK3β activity were inhibited, result in β-Catenin accumulated in the nucleus. CONCLUSION: In conclusion, these results demonstrated that PRDX2 plays a pivotal role in regulating the proliferation of DMSCs, and this is closely related to the AKT/glycogen synthase kinase 3 beta/β-catenin signaling pathway. Copyright
Authors: Qutuba G Karwi; Cory S Wagg; Tariq R Altamimi; Golam M Uddin; Kim L Ho; Ahmed M Darwesh; John M Seubert; Gary D Lopaschuk Journal: Cardiovasc Diabetol Date: 2020-12-07 Impact factor: 9.951