지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2011.1
- 수록면
- 684 - 692 (9page)
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초록· 키워드
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Recent epidemiologic studies clearly showed that early intensive glucose control has a legacy effect for preventing diabetic macrovascular complications.
However, the cellular and molecular processes by which high glucose leads to macrovascular complications are poorly understood. Vascular smooth muscle cell (VSMC) dysfunction due to high glucose is a characteristic of diabetic vascular complications. Activation of nuclear factor-κB (NF-κB) may play a key role in the regulation of inflammation and proliferation of VSMCs.
We examined whether VSMC proliferation and plasminogen activator inhibitor-1 (PAI-1) expression induced by high glucose were mediated by NF-κB activation.
Also, we determined whether selective inhibition of NF-κB would inhibit proliferation and PAI-1 expression in VSMCs. VSMCs of the aorta of male SD rats were treated with various concentrations of glucose (5.6,11.1, 16.7, and 22.2 mM) with or without an inhibitor of NF-κB or expression of a recombinant adenovirus vector encoding an IκB-α mutant (Ad-IκBαM). VSMC proliferation was examined using an MTT assay. PAI-1 expression was assayed by real-time PCR and PAI-1 protein in the media was measured by ELISA. NF-κB activation was determined by immunohistochemical staining, NF-κB reporter assay, and immunoblotting.
We found that glucose stimulated VSMC proliferation and PAI-1 expression in a dose-dependent manner up to 22.2 mM. High glucose (22.2 mM) alone induced an increase in NF-κB activity. Treatment with inhibitors of NF-κB such as MG132, PDTC or expression of Ad-IκB-αM in VSMCs prevented VSMC proliferation and PAI-1 expression induced by high glucose. In conclusion,inhibition of NF-κB activity prevented high glucose-induced VSMC proliferation and PAI-1expression.
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등록된 정보가 없습니다.
참고문헌 (23)
참고문헌 신청
Brand K / 1996 / Activated transcription factor nuclear factor-kappa B is present in the atherosclerotic lesion / J Clin Invest 97 : 1715 ~ 1722
Brand K / 1997 / Role of nuclear factor-κB in atherosclerosis / Exp Physiol 82 : 297 ~ 304
Breuss JM / 2002 / Activation of nuclear factor-kappa B significantly contributes to lumen loss in a rabbit iliac artery balloon angioplasty model / Circulation 105 : 633 ~ 6
Chen Y / 2006 / Augmentation of proliferation of vascular smooth muscle cells by plasminogen activator inhibitor type 1 / Arterioscler Thromb Vasc Biol 26 : 1777 ~ 1783
Cifarelli V / 2008 / Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-kappaB activation in vascular smooth muscle cells / Atherosclerosis 201 : 24
Brand K / 1997 / Role of nuclear factor-κB in atherosclerosis / Exp Physiol 82 : 297 ~ 304
Breuss JM / 2002 / Activation of nuclear factor-kappa B significantly contributes to lumen loss in a rabbit iliac artery balloon angioplasty model / Circulation 105 : 633 ~ 6
Chen Y / 2006 / Augmentation of proliferation of vascular smooth muscle cells by plasminogen activator inhibitor type 1 / Arterioscler Thromb Vasc Biol 26 : 1777 ~ 1783
Cifarelli V / 2008 / Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-kappaB activation in vascular smooth muscle cells / Atherosclerosis 201 : 24
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