Regulation of fibrosis and liver cancer development and progression by platelet C3G

ABSTRACT: Primary liver cancer usually occurs in a context of chronic liver disease (CLD), being associated with fibrosis. Platelets have emerged as important regulators of CLD and liver cancer, although their precise function and mechanism of action need to be clarified. C3G (RapGEF1) regulates platelet activation, adhesion and secretion. Therefore, we have evaluated the role of platelet C3G in chemically-induced fibrosis and liver cancer associated with fibrosis using genetically modified mouse models: mice overexpressing full-length C3G or C3G lacking the catalytic domain in platelets and megakaryocytes, and C3G knockout mice with deletion of C3G in platelets and megakaryocytes (PF4-C3GKO mouse model). Liver immune cell populations have been analyzed as well as regulatory factors involved in regulation of liver fibrosis and cancer. In relation to this, proteins differentially present in platelet-rich -plasma (PRP) from wt and PF4-C3GKO mice have been identified in a wide proteomic analysis. Additionally, differentially secreted proteins by PF4-C3GKO compared to wt platelets have been identified.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Platelet, Blood Plasma

DISEASE(S): Liver Cancer,Liver Disease

SUBMITTER: Concha Gil  

LAB HEAD: Almudena Porras

PROVIDER: PXD050819 | Pride | 2025-05-06

REPOSITORIES: Pride