Low dose monoethyl phthalate (MEP) exposure triggers proliferation by activating PDX-1 at 1.1B4 human pancreatic beta cells
| Autor: | Eylem Taskin, Süleyman Ahbab, Müfide Aydoğan Ahbab, Neslihan Abaci, Fulya Dal, Çağrı Güleç, Sema Sirma Ekmekci, Celal Güven, Handan Akçakaya, Suzan Çinar |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty medicine.drug_class Metabolite medicine.medical_treatment Blotting Western Phthalic Acids Apoptosis 030209 endocrinology & metabolism Type 2 diabetes Toxicology Diethyl phthalate 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Insulin-Secreting Cells Internal medicine Tumor Cells Cultured medicine Humans Insulin Cell Proliferation Homeodomain Proteins Dose-Response Relationship Drug biology Cell Cycle Phthalate Environmental Exposure General Medicine medicine.disease Proliferating cell nuclear antigen 030104 developmental biology Endocrinology chemistry Estrogen Toxicity Trans-Activators biology.protein Food Science |
| Zdroj: | Food and Chemical Toxicology. 93:41-50 |
| ISSN: | 0278-6915 |
| Popis: | Phthalate plasticizers used in a wide range of common plastic products are released into the environment and may pose a risk of increased incidence of type 2 diabetes. In this work, we studied the effects of monoethyl phthalate (MEP), the metabolite of diethyl phthalate, exposure on 1.1B4 human pancreatic beta cells at low doses (1–1000 nM). We showed that MEP treatment induced proliferation in 1.1B4 cells. Also PCNA protein expression levels were increased related to proliferation induction. It has been noted that phthalates can exert estrogen mediated response by interacting with ER. In our study 24 h MEP treatment decreased ERα protein expression level conversely it increased the same protein expression level after 72 h treatment. Also MEP treatment decreased ERβ expression after 72 h at 1.1B4 cells. Our results further show that insulin content of 1.1B4 cells were increased with low dose MEP treatment. Along with our insulin content results, PDX- 1 expression levels were also increased at 1.1B4 cells with MEP treatment. These findings suggest that MEP acts as an estrogenic compound and PPARγ agonist at lower concentrations. Also it should be noted that PDX-1 may be a critical regulator of 1.1B4 cells treated with MEP. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect