Teske K, Erickson N A, Huck A, Dzamukova M, Fulde M, Heinbokel T, Horst D, Klymiuk N, Pastille E, Mekes-Adamczyk A, Löhning M, Gruber A D, Glauben R, Mundhenk L
Institute of Veterinary Pathology, Faculty of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.
MF 3 - Animal Experimental Research and 3r - Methods Development, Research Infrastructure and Information Technology, Robert Koch Institute, Berlin, Germany.
J Mol Med (Berl). 2025 Apr 12. doi: 10.1007/s00109-025-02538-9.
The human chloride channel regulator, calcium-activated (CLCA) 4 is discussed as a driver of epithelial-to-mesenchymal transition as well as a biomarker for colorectal cancer (CRC) and ulcerative colitis. In contrast to humans, the Clca4 gene is duplicated in the mouse, a common model species to study gene functions. However, the relevance of the functional murine Clca4 variants in healthy and diseased intestine is largely unknown. Here, we characterized the spatiotemporal expression patterns of the murine Clca4a and Clca4b genes in the healthy intestinal tract as well as in dextran sulfate sodium (DSS)-induced colitis and colitis-associated colon cancer (CAC) mouse model using RT-qPCR and in situ-hybridization. Similarly, we analyzed expression of the human CLCA4 in healthy, inflamed and cancerous intestinal tracts at single cell level. Murine Clca4a and -4b but not the human CLCA4 were detected in small intestine enterocytes of the respective species. Conversely, healthy colonocytes expressed the human CLCA4 and its murine ortholog Clca4a but not the murine Clca4b. Under inflammatory conditions, de novo expression of Clca4b was observed with both murine homologs abundantly expressed in enterocytes adjacent to ulcerations. Neoplastic colonocytes expressed none or only minimal amounts of the CLCA4 homologs both in humans and mice, whereas adjacent non-neoplastic colonocytes strongly up-regulated the human or both murine homologs, respectively. Our results suggest marked species- and homolog-specific differences in the expression patterns of the three CLCA4 homologs. Moreover, all three seem to play a role in reactive, non-neoplastic colonocytes adjacent to ulcerated and neoplastic lesions. KEY MESSAGES: Human CLCA4 and murine Clca4a, but not Clca4b, are expressed in healthy colonocytes. Inflammation leads to a de novo expression of the murine Clca4b in colonocytes. Human and murine CLCA4 homologs are absent from neoplastic enterocytes. Human and murine CLCA4s are highly expressed in tumor-adjacent, reactive colonocytes.
人类氯离子通道调节剂钙激活蛋白(CLCA)4被认为是上皮-间质转化的驱动因子,也是结直肠癌(CRC)和溃疡性结肠炎的生物标志物。与人类不同,Clca4基因在小鼠中存在重复,小鼠是研究基因功能的常用模式物种。然而,功能性小鼠Clca4变体在健康和患病肠道中的相关性在很大程度上尚不清楚。在这里,我们使用RT-qPCR和原位杂交技术,对小鼠Clca4a和Clca4b基因在健康肠道以及葡聚糖硫酸钠(DSS)诱导的结肠炎和结肠炎相关结肠癌(CAC)小鼠模型中的时空表达模式进行了表征。同样,我们在单细胞水平分析了人类CLCA4在健康、发炎和癌性肠道中的表达。在各自物种的小肠肠细胞中检测到了小鼠Clca4a和-4b,但未检测到人类CLCA4。相反,健康的结肠细胞表达人类CLCA4及其小鼠直系同源基因Clca4a,但不表达小鼠Clca4b。在炎症条件下,观察到Clca4b的从头表达,两种小鼠同源物在溃疡附近的肠细胞中大量表达。肿瘤性结肠细胞在人类和小鼠中均不表达或仅微量表达CLCA4同源物,而相邻的非肿瘤性结肠细胞则分别强烈上调人类或两种小鼠同源物的表达。我们的结果表明,三种CLCA4同源物的表达模式存在明显的物种和同源物特异性差异。此外,所有三种同源物似乎都在溃疡和肿瘤性病变附近的反应性、非肿瘤性结肠细胞中发挥作用。关键信息:人类CLCA4和小鼠Clca4a在健康结肠细胞中表达,但Clca4b不表达。炎症导致结肠细胞中小鼠Clca4b的从头表达。肿瘤性肠细胞中不存在人类和小鼠CLCA4同源物。人类和小鼠CLCA4在肿瘤相邻的反应性结肠细胞中高度表达。