Cytokeratin 19 promoter directs the expression of Cre recombinase in various epithelia of transgenic mice
Metrics: PDF 1284 views | HTML 1477 views | ?
Gui-Feng Zhao1, Shuang Zhao1, Jia-Jie Liu1, Ji-Cheng Wu1, Hao-Yu He1, Xiao-Qing Ding1, Xue-Wen Yu2, Ke-Qiang Huang2, Zhi-Jie Li1, Hua-Chuan Zheng1
1Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China
2Office of Administration, Jinzhou Medical University, Jinzhou 121001, China
Hua-Chuan Zheng, email: email@example.com
Keywords: Cre recombinase, transgenic mouse, cytokeratin 19, PTEN, carcinogenesis
Received: December 01, 2016 Accepted: January 11, 2017 Published: February 17, 2017
Cytokeratin 19 (K19) is expressed in various differentiated cells, including gastric, intestinal and bronchial epithelial cells, and liver duct cells. Here, we generated a transgenic mouse line, K19-Cre, in which the expression of Cre recombinase was controlled by the promoter of K19. To test the tissue distribution and excision activity of Cre recombinase, K19-Cre transgenic mice were bred with Rosa26 reporter strain and a mouse strain that carries PTEN conditional alleles (PTENLoxp/Loxp). At mRNA level, Cre was strongly expressed in the stomach, lung and intestine, while in stomach, lung, and liver at protein level. The immunoreactivity to Cre was strongly observed the cytoplasm of gastric, bronchial and intestinal epithelial cells. Cre activity was detectable in gastric, bronchial and intestinal epithelial cells, according to LacZ staining. In K19-Cre/PTEN Loxp/Loxp mice, PTEN was abrogated in stomach, intestine, lung, liver and breast, the former two of which were verified by in situ PCR. There appeared breast cancer with PTEN loss. These data suggest that K19 promoter may be a useful tool to study the pathophysiological functions of cytokeratin 19-positive cells, especially gastrointestinal epithelial cells. Cell specificity of neoplasia is not completely attributable to the cell-specific expression of oncogenes and cell-specific loss of tumor suppressor genes.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.