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首页> 外文期刊>American Journal of Physiology >Proteinase-activated receptors-1 and 2 induce electrogenic Cl- secretion in the mouse cecum by distinct mechanisms.
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Proteinase-activated receptors-1 and 2 induce electrogenic Cl- secretion in the mouse cecum by distinct mechanisms.

机译：蛋白酶激活的受体1和2通过不同的机制诱导小鼠盲肠中的C1分泌。

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摘要

Proteinase-activated receptors (PAR(1)-PAR(4)) belong to a family of G protein-coupled receptors that are cleaved by proteases. Previous in vitro studies on the mouse large intestine have indicated that PAR(1) and PAR(2) were involved in regulating epithelial ion transport, but that their roles were different between the proximal and distal colon. This present study was done to elucidate the roles of PAR(1) and PAR(2) in regulating anion secretion in the cecum, another segment of the large intestine. A mucosa-submucosal sheet of the mouse cecum was mounted in Ussing chambers, and the short-circuit current (I(sc)) was measured. The addition of a PAR(1)-activating peptide (SFFLRN-NH(2)) to the serosal surface increased I(sc). This increase in I(sc) induced by SFFLRN-NH(2) was partially suppressed by serosal bumetanide and substantially suppressed by mucosal 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and by the removal of Cl(-) from the bathing solution. The I(sc) increase was also substantially suppressed by serosal tetrodotoxin (TTX) and neurokinin-1 receptor antagonist L-703,606 and was partially inhibited by serosal atropine and hexamethonium. The addition of a PAR(2)-activating peptide (SLIGRL-NH(2)) to the serosal surface also induced an increase in I(sc); this increase was partially suppressed by bumetanide and substantially suppressed by NPPB and by the removal of Cl(-), but not by TTX. The expression of mRNA for PAR(1) and PAR(2) was confirmed in the mucosa as determined by RT-PCR. In conclusion, PAR(1) and PAR(2) both induced Cl(-) secretion in the mouse cecum. This secretion mediated by PAR(1) probably occurred by activation of the receptor on the submucosal secretomotor neurons, resulting mainly in the release of tachykinins and activation of the neurokinin-1 receptor, and partly in the release of ACh and activation of the muscarinic and nicotinic receptors. On the other hand, PAR(2)-mediated Cl(-) secretion probably occurred by activating the receptor on the epithelial cells. A variety of proteases would induce fluid secretion mediated by PAR(1) and PAR(2) in the cecum and thereby support bacterial fermentation and participate in mucosal inflammation.
机译：蛋白酶激活受体（PAR（1）-PAR（4））属于被蛋白酶切割的G蛋白偶联受体家族。先前对小鼠大肠进行的体外研究表明，PAR（1）和PAR（2）参与调节上皮离子的转运，但在近端结肠和远端结肠中它们的作用不同。进行本研究的目的是阐明PAR（1）和PAR（2）在调节盲肠（大肠的另一部分）中阴离子分泌中的作用。将小鼠盲肠的粘膜下粘膜下片安装在Ussing室中，并测量短路电流（I（sc））。 PAR（1）激活肽（SFFLRN-NH（2））添加到浆膜表面增加I（sc）。 SFFLRN-NH（2）诱导的I（sc）升高被浆膜布美他尼部分抑制，并被粘膜5-硝基-2-（3-苯基丙基氨基）苯甲酸（NPPB）和去除Cl（- ）从沐浴液中取出。 I（sc）的增加也被浆膜河豚毒素（TTX）和神经激肽-1受体拮抗剂L-703,606基本上抑制，并被浆膜阿托品和六甲铵部分抑制。向浆膜表面添加PAR（2）激活肽（SLIGRL-NH（2））也诱导I（sc）的增加。该增加部分被布美他尼抑制，而被NPPB和去除Cl（-）所抑制，但未被TTX抑制。通过RT-PCR确定了PAR（1）和PAR（2）的mRNA表达。总之，PAR（1）和PAR（2）都诱导小鼠盲肠中Cl（-）的分泌。 PAR（1）介导的这种分泌可能是由于粘膜下分泌运动神经元上的受体激活引起的，主要导致速激肽的释放和神经激肽-1受体的激活，部分导致ACh的释放以及毒蕈碱和乙酰胆碱的激活。烟碱样受体。另一方面，PAR（2）介导的Cl（-）分泌可能是通过激活上皮细胞上的受体而发生的。多种蛋白酶会诱导盲肠中PAR（1）和PAR（2）介导的液体分泌，从而支持细菌发酵并参与粘膜炎症。

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