Expression profiling of endothelial cells from old (12 months) and very old (18 months) homozygous Jak2 R1063H mice and wild-type controls

To investigate the biological role of the germline JAK2-R1063H mutation, which may contribute to susceptibility and pathogenesis of myeloproliferative neoplasms, we generated a mouse model by introducing the R1063H variant into the endogenous Jak2 locus using CRISPR/Cas9 genome editing. This model allowed us to explore not only hematopoietic but also non-hematopoietic compartments potentially affected by the mutation. Given the ongoing debate regarding the presence and functional impact of somatic JAK2-V617F in endothelial cells — and their possible involvement in thrombotic complications — we specifically examined whether Jak2-R1063H in endothelial cells drives similar pathogenic phenotype. Therefore, we isolated lung endothelial cells (CD45?/CD31?) from 12- and 18-month-old Jak2-R1063H and wild-type mice and conducted gene expression profiling.