Itgb3-KO Mouse

Itgb3, also known as integrin β3, is a cell adhesion molecule. It plays crucial roles in cell movement and is involved in multiple signaling pathways, such as MAPK and VEGF [1]. Itgb3 is important in various biological processes including cell proliferation, migration, invasion, and adhesion, and is thus relevant in normal physiological functions as well as disease conditions. Mouse models have been valuable for studying its functions [3].

In osteosarcoma, Itgb3 knockout cells showed decreased proliferation and migration, related to increased apoptosis and slowed cell cycle progression. Itgb3 was positively correlated with cisplatin resistance in cells and tumor xenografts, functioning through the MAPK and VEGF signaling pathways [1]. In Itgb3 -integrin -deficient (Itgb3 -/-) mice, platelets had impaired functions like fibrinogen binding, aggregation, adhesion, or spreading. These mice also had decreased platelet count, microcytic hypochromic anemia, and splenomegaly, but this mouse model couldn't fully simulate patients with Glanzmann thrombasthenia [3]. In preeclampsia, Itgb3 expression was lower in placental tissue, and in HTR8/SVneo cells, it enhanced proliferation, migration, invasion, and adhesion while inhibiting apoptosis [2]. In lung adenocarcinoma, Itgb3 -enriched extracellular vesicles promoted bone metastasis by facilitating osteoclastogenesis and establishing an osteoclastic pre-metastatic niche [4].

In conclusion, Itgb3 is essential for cell-related functions like proliferation, migration, and adhesion. Studies using Itgb3 knockout mouse models have revealed its roles in diseases such as osteosarcoma, providing insights into disease mechanisms and potential therapeutic targets [1,3]. It also has implications in pregnancy-related conditions like preeclampsia and in cancer metastasis, highlighting its broad significance in different biological contexts.

References:

1. Li, Qian, Chen, Guangyou, Jiang, Huachai, Xu, Houping, Li, Sen. 2023. ITGB3 promotes cisplatin resistance in osteosarcoma tumors. In Cancer medicine, 12, 8452-8463. doi:10.1002/cam4.5585. https://pubmed.ncbi.nlm.nih.gov/36772869/

2. Li, Chunyan, Meng, Yanan, Zhou, Beibei, Lv, Mingming, Long, Wei. 2024. ITGB3 is reduced in pregnancies with preeclampsia and its influence on biological behavior of trophoblast cells. In Molecular medicine (Cambridge, Mass.), 30, 275. doi:10.1186/s10020-024-01050-z. https://pubmed.ncbi.nlm.nih.gov/39721996/

3. Li, Dongya, Peng, Jie, Li, Tiantian, Chen, Min, Shi, Xiaofeng. 2021. Itgb3-integrin-deficient mice may not be a sufficient model for patients with Glanzmann thrombasthenia. In Molecular medicine reports, 23, . doi:10.3892/mmr.2021.12088. https://pubmed.ncbi.nlm.nih.gov/33880575/

4. Qiu, Rong, Deng, Yan, Lu, Yue, Huang, Qin, Du, Yuzhen. 2024. ITGB3-enriched extracellular vesicles mediate the formation of osteoclastic pre-metastatic niche to promote lung adenocarcinoma bone metastasis. In Molecular carcinogenesis, 63, 2190-2204. doi:10.1002/mc.23803. https://pubmed.ncbi.nlm.nih.gov/39136603/