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首页> 外文期刊>American Journal of Physiology >Dextran sulfate sodium-induced chronic colitis attenuates Ca~(2+)-activated Cl secretion in murine colon by downregulating TMEM16A
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Dextran sulfate sodium-induced chronic colitis attenuates Ca~(2+)-activated Cl secretion in murine colon by downregulating TMEM16A

机译：耐氧化碳钠诱导的慢性结肠炎衰减Ca〜（2 +） - 通过下调TMEM16A激活鼠结肠中的分泌物

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Attenuated Ca~(2+)-activated Cl~- secretion has previously been observed in the model of dextran sulfate sodium (DSS)-induced colitis. Prior studies have implicated dysfunctional muscarinic signaling from basolateral membranes as the potential perpetrator leading to decreased Ca~(2+)-activated Cl secretion. However, in our chronic model of DSS-colitis, cholinergic receptor muscarinic 3 (Chrm3) transcript (1.028 ?0.12 vs. 1.029 ?0.27, P >0.05) and CHRM3 protein expression (1.021 ?.24 vs. 0.928 + 0.09, P >0.05) were unchanged. Therefore, we hypothesized that decreased carbachol (CCH)-stimulated Cl~- secretion in DSS-induced colitis could be attributed to a loss of Ca~(2+)-activated Cl~- channels (CaCC) in apical membranes of colonic epithelium. To establish this chemically-induced colitis, Balb/C mice were exposed to 4% DSS for five alternating weeks to stimulate a more moderate, chronic colitis. Upon completion of the protocol, whole thickness sections of colon were mounted in an Ussing chamber under voltage-clamp conditions. DSS-induced colitis demonstrated a complete inhibition of basolateral administration of CCH-stimulated Cl~- secretion that actually displayed a reversal in polarity (15.40 ?2.22 糀/cm~2 vs. -2.47 ?0.25 糀/cm~2). Western blotting of potential CaCCs, quantified by densi-tometric analysis, demonstrated no change in bestrophin-2 and cystic fibrosis transmembrane regulator, whereas anoctamin-1 [ANO1, transmembrane protein 16A (TMEM16A)] was significantly down-regulated (1.001 ?0.13 vs. 0.510 ?0.12, P < 0.05). Our findings indicate that decreased expression of TMEM16A in DSS-induced colitis contributes to the decreased Ca~(2+)-activated Cl secretion in murine colon.
机译：衰减的Ca〜（2 +） - 先前已在葡聚糖硫酸钠（DSS）诱导的结肠炎模型中观察到活化的Cl〜 - 分泌。先前的研究与基底外膜有影响的功能障碍毒蕈碱信号，因为潜在的肇事者导致CA〜（2 +）激活的Cl分泌。然而，在我们的DSS-结肠炎的慢性模型中，胆碱能受体肌肉蛋白3（CHRM3）转录物（1.028〜12.12与1.029〜0.27，p> 0.05）和CHRM3蛋白表达（1.021〜24 vs.0.928 + 0.09，P> 0.05）不变。因此，我们假设DSS诱导的结肠炎中的降低的卡巴醇（CCH）-Actimulation的Cl〜 - 分泌物可归因于结肠上皮的顶端膜中的Ca〜（2 +）激活的Cl〜 - 通道（CACC）的损失。为了建立这种化学诱导的结肠炎，将BALB / C小鼠暴露于4％DSS，以刺激更温和的慢性结肠炎。在完成方案后，在电压 - 夹紧条件下，将结肠的整个厚度部分安装在USSing室。 DSS诱导的结肠炎表明，对基石刺激的CCH刺激的CL〜 - 分泌的完全抑制，实际上展示了极性的反转（15.40？2.22×/ cm〜2与-2.47？0.25×/ cm〜2）。潜在的CACCS的蛋白质印迹，通过抗体分析量化量化，表现出嗜碱素-2和囊性纤维化跨膜调节剂的变化，而Anoctamin-1 [AnO1，跨膜蛋白16a（TMem16a）]显着下调（1.001？0.13 Vs 。0.510？0.12，P <0.05）。我们的研究结果表明，DSS诱导的结肠炎中TMEM16A的表达降低有助于鼠结肠中的CA〜（2 +）激活的CL分泌。

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