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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Liu, Rui Yu, Bo Liu, Jian-Xiu Dong, Chao Li, Song-Jian Li, Chen-Tian |
| Description | Author Affiliation: Li CT ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.); Liu JX ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.); Yu B ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.); Liu R ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.); Dong C ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.); Li SJ ( Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.) |
| Abstract | The modification of Wnt and Notch signaling pathways by hypoxia, and its association with osteoblast proliferation and apoptosis remain to be fully elucidated. To investigate Wnt-Notch crosstalk, and its role in hypoxia-induced osteoblast proliferation and apoptosis regulation, the present study investigated the effects of cobaltmimicked hypoxia on the mouse pre-osteoblast-like cell line, MC3T3E1, when the Notch signals were repressed using a γsecretase inhibitor DAPT. The data showed that the cobaltmimicked hypoxia suppressed cell proliferation under normal conditions, but increased cell proliferation under conditions of Notch repression, in a concentrationdependent manner. The results of western blot and reverse transcriptionquantitative polymerase chain reaction analyses showed that the cobalt treatment increased the levels of activated ßcatenin protein and the expression levels of the target genes, axis inhibition protein 2 and myelocytomatosis oncogene, under DAPTinduced Notch repression. However, no significant changes were found in the expression levels of the Notch intracellular domain protein or the Notch target gene, hes1. In a ßcatenin geneknockdown experiment, the proliferation of the MC3T3E1 cells under hypoxia were decreased by DAPT treatment, and knockdown of the expression of hypoxiainducible factor1 (HIF1 ) suppressed the cobaltinduced increase in Wnt target gene levels. No significant difference in cell proliferation rate was found following DAPT treatment when the expression of HIF1 was knocked down. The results of the present study showed the opposing effects of Wnt and Notch signaling under cobaltmimicked hypoxia, which were partially regulated by HIF1 , The results also showed that osteoblast proliferation was dependent on Wnt-Notch signal crosstalk. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2016.5324 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 14 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2016-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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