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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kim, Chun-Ho Lee, Myung Joo Lee, Ok-Kyu Lee, Yu Na Lee, Kee-Ho Bae, Seunghee Ahn, Kyu Joong Cha, Hwa Jun Lim, Kyung Mi An, Sungkwan |
| Description | Author Affiliation: Lee MJ ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.); Cha HJ ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.); Lim KM ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.); Lee OK ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.); Bae S ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.); Kim CH ( Korea Institute of Radiological and Medical Sciences, Seoul 139706, Republic of Korea.); Lee KH ( Korea Institute of Radiological and Medical Sciences, Seoul 139706, Republic of Korea.); Lee YN ( Department of Dermatology, Konkuk University School of Medicine, Seoul 143729, Republic of Korea.); Ahn KJ ( Department of Dermatology, Konkuk University School of Medicine, Seoul 143729, Republic of Korea.); An S ( Korea Institute for Skin and Clinical Sciences and MolecularTargeted Drug Research Center, Konkuk University, Seoul 143701, Republic of Korea.) |
| Abstract | Clinical evidence has demonstrated that the accumulation of 5 -dihydrotestosterone (DHT) in dermal papilla cells (DPCs) is implicated in androgenetic alopecia. Whether this accumulation in DHT may have direct cellular effects leading to androgenetic alopecia remains to be elucidated. The present study aimed to determine whether DHT affects cell growth, cell cycle arrest, cell death, senescence and the induction of reactive oxygen species (ROS), and whether these effects are mediated by microRNA (miRNA)-dependent mechanisms. The cell viability and cell cycle were determined, levels of ROS were examined and senescence-associated ß-galactosidase assays were performed in normal human DPCs (nHDPCs). Furthermore, miRNA expression profiling was performed using an miRNA microarray to determine whether changes in the expression levels of miRNA were associated with the cellular effects of DHT. The results revealed that DHT decreased cell growth by inducing cell death and G2 cell cycle arrest, and by increasing the production of ROS and senescence in the nHDPCs. In addition, 55 miRNAs were upregulated and 6 miRNAs were downregulated in the DHT-treated nHDPCs. Bioinformatic analysis demonstrated that the putative target genes of these upregulated and downregulated miRNAs were involved in cell growth, cell cycle arrest, cell death, senescence and the production of ROS. Specifically, the target genes of five highly upregulated and downregulated miRNAs were identified and were associated with the aforementioned effects of DHT. These results demonstrated that the expression of miRNA was altered in the DHT-treated nHDPCs and suggest the potential mechanisms of DHT-induced cell growth repression, cell cycle arrest, cell death, senescence and induction of ROS. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 12 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2015-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Dermis Drug Effects Dihydrotestosterone Pharmacology Gene Expression Regulation Micrornas Genetics Apoptosis Cell Aging Cell Cycle Checkpoints Cell Line Cell Proliferation Cell Survival Cytology Metabolism Genes, Reporter Oligonucleotide Array Sequence Analysis Reactive Oxygen Species Agonists Signal Transduction Beta-galactosidase Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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