Brain-Derived Neurotrophic Factor Regulates Ishikawa Cell Proliferation through the TrkB-ERK1/2 Signaling Pathway
Autor: | XinYu Xiang, Zijiao Zhao, Qiaoge Niu, Yuwen Huang, Meng Tian, Xu Zhou, Tariq Iqbal, Chunjin Li, Maosheng Cao, Chenfeng Yuan |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Cell Survival lcsh:QR1-502 Carbazoles TrkB-ERK1/2 signaling pathway Tropomyosin receptor kinase B Biochemistry lcsh:Microbiology Article Indole Alkaloids 03 medical and health sciences Endometrium 0302 clinical medicine Cyclin D1 Neurotrophic factors Ishikawa cell Cell Line Tumor Cyclins Humans Receptor trkB Viability assay RNA Small Interfering Molecular Biology Cell Proliferation Brain-derived neurotrophic factor Flavonoids Mitogen-Activated Protein Kinase 1 Membrane Glycoproteins Mitogen-Activated Protein Kinase 3 Estradiol Chemistry Brain-Derived Neurotrophic Factor Cell biology Reverse transcription polymerase chain reaction 030104 developmental biology Cyclin E2 BDNF nervous system Gene Expression Regulation 030220 oncology & carcinogenesis Female Estradiol-17β Signal transduction Mitogen-Activated Protein Kinases Signal Transduction |
Zdroj: | Biomolecules Volume 10 Issue 12 Biomolecules, Vol 10, Iss 1645, p 1645 (2020) |
ISSN: | 2218-273X |
DOI: | 10.3390/biom10121645 |
Popis: | (1) Background: Endometrial regulation is a necessary condition for maintaining normal uterine physiology, which is driven by many growth factors. Growth factors produced in the endometrium are thought to be related to the proliferation of endometrial cells induced by estradiol-17&beta (E2). In this study, we found that E2 can induce the secretion of brain-derived neurotrophic factor (BDNF) in Ishikawa cells (the cells of an endometrial cell line). Furthermore, Ishikawa cells were used in exploring the regulatory role of BDNF in endometrial cells and to clarify the potential mechanism. (2) Methods: Ishikawa cells were treated with different concentrations of BDNF (100, 200, 300, 400, and 500 ng/mL). The mRNA expression levels of various proliferation-related genes were detected through quantitative reverse transcription polymerase chain reaction, and the expression of various proliferation-related genes was detected by knocking out BDNF or inhibiting the binding of BDNF to its receptor TrkB. The expression levels of various proliferation-related genes were detected by performing Western blotting on the TrkB-ERK1/2 signaling pathway. (3) Results: Exogenous BDNF promoted the growth of the Ishikawa cells, but the knocking down of BDNF or the inhibition of TrkB reduced their growth. Meanwhile, BDNF enhanced cell viability and increased the expression of proliferation-related genes, including cyclin D1 and cyclin E2. More importantly, the BDNF-induced proliferation of the Ishikawa cells involved the ERK1/2 signaling pathway. (4) Conclusions: The stimulating effect of exogenous E2 on the expression of BDNF in the uterus and the action of BDNF promoted the proliferation of the Ishikawa cells through the TrkB-ERK1/2 signal pathway. |
Databáze: | OpenAIRE |
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