Vascular dysfunction is the primary cause of symptom onset in a mouse  model of oxaliplatin-induced peripheral neuropathy: comparison of gene expression in mice injected with Oxaliplatine or control solution [BHN-OXA_A2020]
Oxaliplatin-induced peripheral neuropathy (OIPN) is an adverse side effect of this chemotherapy used for gastrointestinal cancers. The continuous pain experienced by OIPN patients often result in the reduction or discontinuation of chemotherapy, thereby affecting patient survival. Several pathogenic mechanisms involving sensory neurons were shown to participate in the occurrence of OIPN symptoms. However, the dysfunction of the blood-nerve barrier as a source of nerve alteration had not been thoroughly explored. To characterise the vascular contribution to OIPN symptoms, we undertook two comparative transcriptomic analyses from mouse purified brain and sciatic nerve blood vessels (BVs), and nerve BVs after oxaliplatin or control administration. The dataset provided here show raw data obtained when gene expression regulation was assessed by transcriptomic analyses where we compared purified blood vessels (endothelial cells and mural cells incl. smooth muscle cells and pericytes) from sciatic nerves of mice intraveinously injected with control (sham) or oxaliplatin (oxa) solution. Overall design: Comparison of gene expression in mice injected with Oxaliplatine or control solution The mouse strain for both experiments (GSE255096 and GSE255097) was C57BL/6.