Adiponectin increases secretion of rat submandibular gland via adiponectin receptors-mediated AMPK signaling.
Adiponectin increases secretion of rat submandibular gland via adiponectin receptors-mediated AMPK signaling.
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脂联素通过脂联素受体介导的 AMPK 信号增加大鼠颌下腺的分泌
DOI：
10.1371/journal.pone.0063878
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Yu GY
中科院分区：
文献类型：
--
作者：
Ding C;Li L;Su YC;Xiang RL;Cong X;Yu HK;Li SL;Wu LL;Yu GY
脂联素和脂联素受体（AdipoR 1/2）在多种组织中表达，并参与多种功能的调节，如能量代谢和炎症反应。然而，脂联素和AdipoRs在下颌下腺中的作用尚未得到充分评价。在本研究中，我们发现，脂联素和AdipoR 1/2的mRNA和蛋白质的表达在大鼠下颌下腺和SMG-C6细胞系中，通过RT-PCR和Western blot分析证明。免疫荧光染色显示脂联素主要分布在腺泡细胞的胞浆中，而AdipoR 1/2主要分布在腺泡细胞的胞膜上。全长脂联素（fAd）或球状脂联素（gAd）灌注在离体大鼠下颌下腺的唾液流量显着增加。5-氨基咪唑-4-甲酰胺-1-4-呋喃核糖苷（AICAR），一种腺苷单磷酸活化蛋白激酶（AMPK）激活剂，也增加唾液分泌。fAd、gAd和AICAR均增加了灌流的下颌下腺顶端紧密连接的平均宽度，并降低了SMG-C6细胞的跨上皮电阻（TER），表明脂联素通过调节细胞旁通透性促进分泌。fAd和gAd增加p-AMPK水平，而AraA，AMPK拮抗剂，取消fAd和gAd引起的分泌，紧密连接超微结构和TER的变化。此外，AdipoR 1和AdipoR 2都是fAd或gAd诱导的p-AMPK和TER反应所必需的，这表明AdipoR 1或AdipoR 2敲低后的抑制以及通过RNA干扰共敲低AdipoRs。我们的研究结果表明，脂联素功能作为一个促进唾液分泌的大鼠下颌下腺通过激活AdipoRs，AMPK，和细胞旁通透性。
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-4-carboxamide-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.
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影响因子：
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作者：
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通讯作者：
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