PEDF and PEDF-derived peptide 44mer inhibit oxygen-glucose deprivation-induced oxidative stress through upregulating PPARγ via PEDF-R in H9c2 cells
| Autor: | Jiajun Pan, Zhiwei Liu, Hao Zhang, Wei Zhuang, Zhimin Li, Tengteng Wei, Zhongming Zhang, Hongyan Dong, Qiuhua Guan, Huazhu Cui |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Receptors Neuropeptide Small interfering RNA Biophysics Peroxisome proliferator-activated receptor Biology medicine.disease_cause Biochemistry Cell Line 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine PEDF Lysophosphatidic acid medicine Humans Myocytes Cardiac Nerve Growth Factors Eye Proteins Molecular Biology Serpins chemistry.chemical_classification TUNEL assay Cell Biology Molecular biology Up-Regulation Molecular Weight Oxygen PPAR gamma Oxidative Stress 030104 developmental biology Glucose chemistry Apoptosis Signal transduction Peptides 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Biochemical and biophysical research communications. 472(3) |
| ISSN: | 1090-2104 |
| Popis: | Pigment epithelial-derived factor (PEDF) is a glycoprotein with broad biological activities including inhibiting oxygen-glucose deprivation(OGD)-induced cardiomyocytes apoptosis through its anti-oxidative properties. PEDF derived peptide-44mer shows similar cytoprotective effect to PEDF. However, the molecular mechanisms mediating cardiomyocytes apoptosis have not been fully established. Here we found that PEDF and 44mer decreased the content of ROS. This content was abolished by either PEDF-R small interfering RNA (siRNA) or PPARγ antagonist. The level of Lysophosphatidic acid (LPA) and phospholipase A2 (PLA2) was observed as drawn from the ELISA assays. PEDF and 44mer sequentially induced PPARγ expression was observed both in qPCR and Western blot assays. The level of LPA and PLA2 and PPARγ expression increased by PEDF and 44mer was significantly attenuated by PEDF-R siRNA. However, PEDF and 44mer inhibited the H9c2 cells and cultured neonatal rat myocardial cells apoptosis rate. On the other hand, TUNEL assay and cleavage of procaspase-3 showed that PEDF-R siRNA or PPARγ antagonist increased the apoptosis again. We conclude that under OGD condition, PEDF and 44mer reduce H9c2 cells apoptosis and inhibit OGD-induced oxidative stress via its receptor PEDF-R and the PPARγ signaling pathway. |
| Databáze: | OpenAIRE |
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