Chung Yoohwa, Saitoh Yurika, Hayashi Tetsuro, Fukui Yuya, Terada Nobuo, Seiki Motoharu, Murakami Yoshinori, Sakamoto Takeharu
Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Center for Medical Education, Teikyo University of Science, Adachi-ku, Tokyo, 120-0045, Japan.
Biochem Biophys Rep. 2020 Dec 8;24:100872. doi: 10.1016/j.bbrep.2020.100872. eCollection 2020 Dec.
Munc-18 interacting protein 3 (Mint3) is an activator of hypoxia-inducible factor-1 in cancer cells, macrophages, and cancer-associated fibroblasts under pathological conditions. However, exactly which cells highly express Mint3 in vivo and whether Mint3 depletion affects their physiological functions remain unclear. Here, we surveyed mouse tissues for specific expression of Mint3 by comparing Mint3 expression in wild-type and Mint3-knockout mice. Interestingly, immunohistochemical analyses revealed that Mint3 was highly expressed in islet cells of the pancreas, distal tubular epithelia of the kidney, choroid plexus ependymal cells of the cerebrum, medullary cells of the adrenal gland, and epithelial cells of the seminal gland. We also studied whether Mint3 depletion affects the physiological functions of the islets and kidneys. Mint3-knockout mice did not show any abnormalities in glucose-tolerance and urine-biochemical tests, indicating that Mint3 depletion was compensated for in these organs. Thus, loss of Mint3 might be compensated in the islets and kidneys under physiological conditions in mice.
Munc-18相互作用蛋白3（Mint3）是病理条件下癌细胞、巨噬细胞和癌症相关成纤维细胞中缺氧诱导因子-1的激活剂。然而，在体内究竟哪些细胞高度表达Mint3，以及Mint3缺失是否会影响它们的生理功能仍不清楚。在此，我们通过比较野生型和Mint3基因敲除小鼠中Mint3的表达，来研究小鼠组织中Mint3的特异性表达。有趣的是，免疫组织化学分析显示，Mint3在胰腺的胰岛细胞、肾脏的远端肾小管上皮细胞、大脑的脉络丛室管膜细胞、肾上腺的髓质细胞以及精囊的上皮细胞中高度表达。我们还研究了Mint3缺失是否会影响胰岛和肾脏的生理功能。Mint3基因敲除小鼠在葡萄糖耐量和尿液生化测试中未表现出任何异常，表明在这些器官中Mint3缺失得到了代偿。因此，在小鼠的生理条件下，Mint3的缺失可能在胰岛和肾脏中得到了代偿。
