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Claudin-4 is required for AMPK-modulated paracellular permeability in submandibular gland cells
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
2014-12-01
DOI10.1093/jmcb/mju048
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
资助者National Natural Science Foundation of China ; National Natural Science Foundation of China
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
资助者National Natural Science Foundation of China ; National Natural Science Foundation of China
WOS记录号WOS:000348600100005
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/60937
专题北京大学口腔医学院
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
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GB/T 7714
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.
APA Xiang, Ruo-Lan.,Mei, Mei.,Cong, Xin.,Li, Jing.,Zhang, Yan.,...&Yu, Guang-Yan.(2014).Claudin-4 is required for AMPK-modulated paracellular permeability in submandibular gland cells.JOURNAL OF MOLECULAR CELL BIOLOGY,6(6),486-497.
MLA Xiang, Ruo-Lan,et al."Claudin-4 is required for AMPK-modulated paracellular permeability in submandibular gland cells".JOURNAL OF MOLECULAR CELL BIOLOGY 6.6(2014):486-497.
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