Enhancement of FGF-1 release along with cytosolic proteins from rat astrocytes by hydrogen peroxide

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• 作者：Jin-ichi Ito ; Yuko Nagayasu ; Mariko Hoshikawa ; Koichi H. kato ; Yutaka Miura ; Kiyofumi Asai ; Hideki Hayashi ; Shinji Yokoyama ; Makoto Michikawa
• 关键词：BBB ; blood brain barrier ; apo ; apolipoprotein ; DPBS ; Dulbecco's phosphate-buffered saline ; BSA ; bovine serum albumin ; CNS ; central nervous system ; CSF ; cerebrospinal fluid ; DMEM ; Dulbecco's modified Eagle's medium ; FGF-1 ; fibroblast growth factor 1 ; FCS
• 刊名：Brain Research
• 出版年：2013
• 出版时间：19 July, 2013
• 年：2013
• 卷：1522
• 期：Complete
• 页码：12-21
• 全文大小：1657 K

文摘

We previously observed that the production and release of fibroblast growth factor (FGF-1) are increased in rat astrocytes during in vitro long-term culture, that FGF-1 enhances the generation of apoE-containing high density lipoproteins (apoE/HDL), and that the wound healing of brain cryoinjury delays in apoE-deficient mouse. The detail mechanism underlying these phenomena remains unknown. In this study, we examined effects of oxidative stress on release of FGF-1 from cultured rat astrocytes.

The treatment of rat astrocytes with 100 ¦ÌM hydrogen peroxide (H₂O₂) for 10 min enhanced FGF-1 release without inducing apoptosis. The conditioned medium prepared from the cells cultured in a fresh medium after the treatment with H₂O₂ had the FGF-1-like activities, which enhanced cholesterol synthesis, signalings to phosphorylate Akt and ERK, and apoE secretion. The oxidative stress induced by H₂O₂ enhanced the release of cytosolic proteins such as HSP70 and HSP90 in addition to FGF-1. Antioxidants such as ascorbic acid and ebselen suppressed the release of cytosolic proteins induced by H₂O₂ treatment. The addition of lipoproteins such as low density lipoproteins (LDL), furthermore, canceled H₂O₂-induced release of FGF-1 and cytosolic proteins. Proteolysis of cytosolic proteins in the H₂O₂-treated rat astrocytes was enhanced in the presence of exogenous trypsin, which was attenuated by the pretreatment with LDL, suggesting that H₂O₂ increases the permeability of the membrane of cells, which was prevented by the addition of lipoproteins. These findings suggest that oxidative stress is one of the candidates which triggers FGF-1 release from astrocytes in the brain, and that the lipid homeostasis in the cell membrane may regulate H₂O₂-induced release of FGF-1.