Saa2-KO Mouse

Saa2 is a member of the Serum Amyloid A (SAA) protein family. SAA proteins are small, well-conserved in mammalian evolution, and are mainly synthesized in the liver. Saa2, along with SAA1, is a prominent member of the acute-phase response, and their serum levels rise significantly after trauma, infection, etc. Saa2 is lipophilic and contributes to high-density lipoproteins and cholesterol transport. It also participates in various biological processes such as tissue remodeling, immune regulation, and has been implicated in many diseases [1].

In a mouse model of intrauterine inflammation, placental Saa2 increased significantly. Maternal inhibition of Saa2 using siSaa2 markedly decreased preterm birth and downregulated the increased placental expression of pro-inflammatory cytokines Il1β, Il6, and Tnfα, suggesting Saa2 may be a key factor in the mechanism of preterm birth [2]. In another study, Lactobacillus intestinalis decreased C/EBPA-driven gut epithelial Saa2 production, which in turn impaired Th17 cell differentiation, indicating Saa2's role in colitis-related Th17 response [3].

In conclusion, Saa2 is involved in important biological functions including acute-phase response, lipid transport, and immune regulation. Studies using gene-targeting mouse models, like siRNA-mediated Saa2 silencing, have revealed its role in diseases such as preterm birth and colitis, providing potential therapeutic targets for these conditions.

References:

1. Sack, George H. . Serum Amyloid A (SAA) Proteins. In Sub-cellular biochemistry, 94, 421-436. doi:10.1007/978-3-030-41769-7_17. https://pubmed.ncbi.nlm.nih.gov/32189310/

2. Liu, Yang, Liu, Jin, Liu, Anguo, Burd, Irina, Lei, Jun. 2022. Maternal siRNA silencing of placental SAA2 mitigates preterm birth following intrauterine inflammation. In Frontiers in immunology, 13, 902096. doi:10.3389/fimmu.2022.902096. https://pubmed.ncbi.nlm.nih.gov/36211368/

3. Wang, Qi-Wen, Jia, Ding-Jia-Cheng, He, Jia-Min, Wang, Liang-Jing, Chen, Shu-Jie. 2023. Lactobacillus Intestinalis Primes Epithelial Cells to Suppress Colitis-Related Th17 Response by Host-Microbe Retinoic Acid Biosynthesis. In Advanced science (Weinheim, Baden-Wurttemberg, Germany), 10, e2303457. doi:10.1002/advs.202303457. https://pubmed.ncbi.nlm.nih.gov/37983567/