The Role of Calcium-Binding Protein S100g (CalbindinD-9K) and Annexin A10 in Acute Pancreatitis.
The Role of Calcium-Binding Protein S100g (CalbindinD-9K) and Annexin A10 in Acute Pancreatitis.
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钙结合蛋白 S100g (CalbindinD-9K) 和膜联蛋白 A10 在急性胰腺炎中的作用。
DOI：
10.1016/j.bbrc.2020.03.155
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
Ohnishi H.
中科院分区：
文献类型：
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作者：
Mashima H;Takahashi K;Sekine M;Matsumoto S;Asano T;Uehara T;Fujiwara J;Otake H;Ishii T;Yoshikawa S;Miura T;Koito Y;Kashima H;Matsumoto K;Ohnishi H.
背景我们报道了干扰素调节因子（IRF）2基因敲除（KO）小鼠的胰腺代表了急性胰腺炎的早期阶段，包括调节性胞吐缺陷、细胞内胰蛋白酶激活和自噬紊乱。已经报道了IRF 2 KO胰腺中显著上调和下调的基因。基因转录本目录包括两种类型的钙结合蛋白（S100钙结合蛋白G [S100 g]和膜联蛋白A10 [Anxa 10]），它们在IRF 2 KO胰腺中高度上调。由于细胞内钙信号在调节胞吐中起着关键作用，其紊乱与胰腺炎有关，我们随后评估了S100 g和Anxa 10在急性pancreatitis. Methods中的作用，我们在野生型小鼠中诱导蛙皮素胰腺炎，并通过qPCR和免疫组化检测这些基因表达的变化。我们构建了过表达S100 g或过表达Anxa 10的AR 42 J细胞（AR 42 J-S100 g，AR 42 J-Anxa 10）。我们研究了淀粉酶分泌的变化，细胞内钙（[Ca 2 +]i），和细胞活力在这些细胞中，当孵育胆囊收缩素（CCK. ResultsThe S100 g和Anxa 10的表达增加，在天蓝色诱导胰腺炎。腺泡对S100 g呈斑片状染色，腺泡胞液对Anxa 10呈均匀但弱染色。100 pM CCK-8可抑制AR 42 J-S100 g细胞内[Ca ~（2+）]i的升高，降低淀粉酶的分泌。这些作用在AR 42 J-Anxa 10细胞中较弱。结论在青色胰腺炎中，S100 g和Anxa 10的表达在腺泡中被诱导。S100 g可能在急性胰腺炎中起钙缓冲作用。
BackgroundWe reported that the pancreas of the interferon-regulatory factor (IRF) 2 knock-out (KO) mouse represents an early phase of acute pancreatitis, including defective regulatory exocytosis, intracellular activation of trypsin, and disturbance of autophagy. The significantly upregulated and downregulated genes in the IRF2 KO pancreas have been reported. The catalogue of gene transcripts included two types of calcium-binding proteins (S100 calcium binding protein G [S100g] and Annexin A10 [Anxa10]), which were highly upregulated in the IRF2 KO pancreas. As the intracellular calcium signal plays a pivotal role in regulatory exocytosis and its disturbance is related to pancreatitis, we then evaluated the role of S100g and Anxa10 in acute pancreatitis.MethodWe induced cerulein-pancreatitis in wild-type mice and examined the changes in the expression of these genes by qPCR and immunohistochemistry. We constructed S100g-overexpressing or Anxa10-overexpressing AR42J cells (AR42J-S100g, AR42J-Anxa10). We examined the changes in amylase secretion, intracellular calcium ([Ca2+]i), and cell viability in these cells, when incubated with cholecystokinin (CCK).ResultsThe expression of S100g and Anxa10 was increased in cerulean-induced pancreatitis. The acini were patchily stained for S100g and the cytosol of acini was evenly but weakly stained for Anxa10. Stimulation with 100pM CCK-8, decreased amylase secretion and inhibited the [Ca2+]i increase in AR42J-S100g cells. These effects were weak in AR42J-Anxa10 cells. Cell viability was not changed by incubation with cerulein.ConclusionIn cerulean pancreatitis, the expression of S100g and Anxa10 was induced in the acini. S100g may work as a Ca2+buffer in acute pancreatitis.