Mir155-KO Mouse

Mir155, also known as microRNA-155, is an important regulator involved in various biological processes and diseases. It plays a role in immune cell development and function, and is associated with inflammation-related pathways [3,5]. Its dysregulation has been linked to conditions such as cancer, bone-related disorders, and vascular diseases, highlighting its biological importance. Genetic models, like KO mouse models, have been crucial in understanding its functions.

In breast cancer, miR155-deficient MMTV-PyMT mice showed reduced tumor burden, with decreased proliferation, increased apoptosis, and an improved tumor microenvironment through modulation of genes related to protumorigenic processes [1]. In osteogenesis, Mir155-KO mice had a high bone mass phenotype, robust bone regeneration, and enhanced osteogenic differentiation of bone marrow stromal stem cells, indicating a catabolic effect of Mir155 on osteogenesis via targeting S1pr1 [2]. In vascular calcification, miR155-/-mice were resistant to vitamin D3-induced vascular calcification, as miR155 deficiency alleviated the reduction of Rictor, increased Akt phosphorylation, and accelerated FOXO3a degradation, reducing vascular smooth muscle cell apoptosis [4].

In conclusion, Mir155 is a key regulator with diverse functions. Model-based research, especially using Mir155 KO mouse models, has revealed its role in breast cancer, osteogenesis, and vascular calcification. Understanding Mir155 can provide insights into the mechanisms of these diseases and potentially offer new therapeutic strategies.

References:

1. McDonald, Sierra J, Cranford, Taryn L, VanderVeen, Brandon N, Fan, Daping, Murphy, E Angela. 2022. miR155 deficiency reduces breast tumor burden in the MMTV-PyMT mouse model. In Physiological genomics, 54, 433-442. doi:10.1152/physiolgenomics.00057.2022. https://pubmed.ncbi.nlm.nih.gov/36121133/

2. Zheng, Zhichao, Wu, Lihong, Li, Zhicong, Jaspers, Richard T, Pathak, Janak L. 2023. Mir155 regulates osteogenesis and bone mass phenotype via targeting S1pr1 gene. In eLife, 12, . doi:10.7554/eLife.77742. https://pubmed.ncbi.nlm.nih.gov/36598122/

3. Yoon, Jeff S J, Wu, Mike K, Zhu, Tian Hao, Chamberlain, Thomas C, Mui, Alice L-F. 2020. Interleukin-10 control of pre-miR155 maturation involves CELF2. In PloS one, 15, e0231639. doi:10.1371/journal.pone.0231639. https://pubmed.ncbi.nlm.nih.gov/32324763/

4. Li, Yong, Sun, Wei, Saaoud, Fatma, Kong, Xiangqing, Fan, Daping. 2020. MiR155 modulates vascular calcification by regulating Akt-FOXO3a signalling and apoptosis in vascular smooth muscle cells. In Journal of cellular and molecular medicine, 25, 535-548. doi:10.1111/jcmm.16107. https://pubmed.ncbi.nlm.nih.gov/33210462/

5. Chen, Siqi, Wang, Long, Fan, Jie, Kuzel, Timothy M, Zhang, Bin. 2014. Host miR155 promotes tumor growth through a myeloid-derived suppressor cell-dependent mechanism. In Cancer research, 75, 519-31. doi:10.1158/0008-5472.CAN-14-2331. https://pubmed.ncbi.nlm.nih.gov/25502838/