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
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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