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Title 

CI- -channel is essential for LDL-induced cell proliferation via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1 in human aortic smooth muscle cells

Authors 

Kyung Sun HeoS W RyooL KimMi-Young NamS T BaekHye Mi LeeAh-Reum LeeSong Kyu ParkYoung Woo ParkC S MyungDong Uk KimKwang Lae Hoe

Publisher 

Springer Verlag (Germany)

Issue Date 

2008

Citation 

Molecules and Cells, vol. 26, no. 5, pp. 468-473

Keywords 

Cl-- channelDIDSEgr-1low-density lipoproteinPI3K2 (2 amino 3 methoxyphenyl)chromone2 morpholino 8 phenylchromone4,4' diisothiocyanatostilbene 2,2' disulfonic acid5 nitro 2 (3 phenylpropylamino)benzoic acidearly growth response factor 1

Abstract 

Low-density lipoprotein (LDL) induces cell proliferation in human aortic smooth muscle cells (hAoSMCs), which may be involved in atherogenesis and intimal hyperplasia. Recent studies have demonstrated that Cl- channels are related to vessel cell proliferation induced by a variety of stimuli. In this study, we investigated a potential role of Cl- channels in the signaling pathway of LDL effects on hAoSMC proliferation with a focus on the activation of Erk1/2-PI3K/Akt and the subsequent upregulation of Egr-1. Cl- channel blockers, DIDS, but neither NPPB nor Furosemide, completely abolished the LDL-induced DNA synthesis and cell proliferation. Moreover, DIDS, but not NPPB, significantly decreased LDL-stimulated Cl- concentration, as judged by flow cytometry analysis using MQAE as a Cl-detection dye. DIDS pretreatment completely abolished the activation of Erk1/2 and PI3K/Akt in a dose-dependent manner that is the hallmark of LDL activation, as judged by Western blot and proliferation assays. Moreover, pretreatment with DIDS (Cl- channel blockers) but not LY294002 (PI3K inhibitors) completely abolished the LDL-induced upregulation of Egr-1 to the same extent as PD98059 (MEK inhibitors to inhibit Erk), as judged by Western blot and luciferase reporter assays. This is the first report, to our knowledge, that DIDS-sensitive Cl- channels play a key role in the LDL-induced cell proliferation of hAoSMCs via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1.

ISSN 

1016-8478

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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