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学科主题: 口腔医学
题名:
Claudin-4 is required for AMPK-modulated paracellular permeability in submandibular gland cells
作者: Xiang, Ruo-Lan1,2; Mei, Mei3; Cong, Xin1,2; Li, Jing3; Zhang, Yan1,2; Ding, Chong4; Wu, Li-Ling1,2; Yu, Guang-Yan3
关键词: AMP-activated protein kinase ; claudin-4 ; tight junction ; paracellular permeability ; submandibular gland
刊名: JOURNAL OF MOLECULAR CELL BIOLOGY
发表日期: 2014-12-01
DOI: 10.1093/jmcb/mju048
卷: 6, 期:6, 页:486-497
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cell Biology
研究领域[WOS]: Cell Biology
关键词[WOS]: TIGHT JUNCTION PROTEINS ; EPITHELIAL-CELLS ; SALIVARY-GLANDS ; BARRIER FUNCTION ; OCCLUDIN ; KINASE ; PHOSPHORYLATION ; ACTIVATION ; EXPRESSION ; MONOLAYERS
英文摘要:

Tight junction plays an important role in mediating paracellular permeability in epithelia. We previously found that activation of AMP-activated protein kinase (AMPK) increased saliva secretion by modulating paracellular permeability in submandibular glands. However, the molecular mechanisms underlying AMPK-modulated paracellular permeability are unknown. In this study, we found that AICAR, an AMPK agonist, increased saliva secretion in the isolated rat submandibular glands, decreased transepithelial electrical resistance (TER), and increased 4 kDa FITC-dextran flux in cultured SMG-C6 cells. AICAR also induced redistribution of tight junction protein claudin-4, but not claudin-1, claudin-3, occludin, or ZO-1, from the cytoplasm to the membrane. Moreover, knockdown of claudin-4 by shRNA suppressed while claudin-4 re-expression restored the TER and 4 kDa FITC-dextran flux responses to AICAR. Additionally, AICAR increased ERK1/2 phosphorylation, and inhibition of ERK1/2 by U0126, an ERK1/2 kinase inhibitor, or by siRNA decreased AICAR-induced TER responses. AICAR induced the serine S199 phosphorylation of claudin-4 and enhanced the interaction of claudin-4 and occludin. Furthermore, pretreatment with U0126 significantly suppressed AMPK-modulated phosphorylation, redistribution, and interaction with occludin of claudin-4. Taken together, these results indicated that claudin-4 played a crucial role in AMPK-modulated paracellular permeability and ERK1/2 was required in AMPK-modulated tight junction barrier function in submandibular gland.

语种: 英语
所属项目编号: 81100763 ; 81271161 ; 81442007
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000348600100005
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60937
Appears in Collections:北京大学口腔医学院_期刊论文

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作者单位: 1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Ctr Salivary Gland Dis,Sch & Hosp Stomatol, Dept Physiol & Pathophysiol,Sch Basic Med Sci, Beijing 100191, Peoples R China
3.Peking Univ, Sch & Hosp Stomatol, Dept Oral & Maxillofacial Surg, Beijing 100081, Peoples R China
4.Peking Univ, Sch & Hosp Stomatol, Cent Lab, Beijing 100081, Peoples R China

Recommended Citation:
Xiang, Ruo-Lan,Mei, Mei,Cong, Xin,et al. Claudin-4 is required for AMPK-modulated paracellular permeability in submandibular gland cells[J]. JOURNAL OF MOLECULAR CELL BIOLOGY,2014,6(6):486-497.
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