Title Adiponectin Increases Secretion of Rat Submandibular Gland via Adiponectin Receptors-Mediated AMPK Signaling
Authors Ding, Chong
Li, Li
Su, Yun-Chao
Xiang, Ruo-Lan
Cong, Xin
Yu, Hong-Kui
Li, Sheng-Lin
Wu, Li-Ling
Yu, Guang-Yan
Affiliation Peking Univ, Sch & Hosp Stomatol, Ctr Salivary Gland Dis, Beijing 100871, Peoples R China.
Peking Univ, Sch & Hosp Stomatol, Ctr Lab, Beijing 100871, Peoples R China.
Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China.
Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China.
Peking Univ, Sch & Hosp Stomatol, Dept Oral & Maxillofacial Surg, Beijing 100871, Peoples R China.
Keywords ACTIVATED PROTEIN-KINASE
EPITHELIAL TIGHT JUNCTIONS
MYOCARDIAL-INFARCTION
CELL MONOLAYERS
DIABETIC-RATS
EXPRESSION
SALIVARY
ASSOCIATION
HYPOADIPONECTINEMIA
PHOSPHORYLATION
Issue Date 2013
Publisher plos one
Citation PLOS ONE.2013,8,(5).
Abstract Adiponectin and adiponectin receptors (AdipoR1/2) are expressed in various tissues and are involved in the regulation of multiple functions such as energy metabolism and inflammatory responses. However, the effect of adiponectin and AdipoRs in submandibular glands has not been fully evaluated. In the present study, we found that mRNA and protein of both adiponectin and AdipoR1/2 were expressed in rat submandibular glands and in the SMG-C6 cell line, as evidenced by RT-PCR and Western blot analysis. Immunofluorescence staining showed that adiponectin was diffused in the cytoplasm, while AdipoR1/2 was concentrated in the membrane of acinar cells. Saliva flow was significantly increased by full length adiponectin (fAd) or globular adiponectin (gAd) perfusion in isolated rat submandibular glands. 5-Aminoimidazole-4carboxamide- 1-4-ribofuranoside (AICAR), an adenosine monophosphate activated protein kinase (AMPK) activator, also increased saliva secretion. fAd, gAd, and AICAR all increased the average width of apical tight junctions in perfused submandibular glands, and decreased transepithelial electrical resistance (TER) in SMG-C6 cells, suggesting that adiponectin promoted secretion by modulating paracellular permeability. fAd and gAd increased p-AMPK levels, while AraA, an AMPK antagonist, abolished fAd- and gAd-induced changes in secretion, tight junction ultrastructure, and TER. Moreover, both AdipoR1 and AdipoR2 were required for fAd- or gAd-induced p-AMPK and TER responses, suggesting from their inhibition following AdipoR1 or AdipoR2 knockdown, and co-knockdown of AdipoRs by RNA interference. Our results suggest that adiponectin functions as a promoter of salivary secretion in rat submandibular glands via activation of AdipoRs, AMPK, and paracellular permeability.
URI http://hdl.handle.net/20.500.11897/163066
ISSN 1932-6203
DOI 10.1371/journal.pone.0063878
Indexed SCI(E)
PubMed
Appears in Collections: 口腔医院

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