Chhiring Sherpa

An endothelial-specific TIE2-L914F mouse model reveals cellular mechanisms of venous malformation progression and recapitulates the patient's response to targeted therapy

This study creates a TIE2-L914F mouse model to study venous malformation progression and shows it responds to rapamycin treatment.

Constitutive, mosaic expression of TIE2 p.L914F during mouse development causes formation of venous malformation

This study shows that mosaic expression of the TIE2 p.L914F mutation during mouse development causes partial embryonic lethality and venous malformation.

Expression of mutant TIE2 p.L914F during mouse development causes embryonic lethality and defects in vascular remodeling

This study shows that the TIE2 p.L914F mutation causes embryonic lethality and vascular defects in mice, highlighting its incompatibility with early vascular development.

Semaphorin 3A and 3F overexpression in TIE2 hyperactive endothelial cells contribute to the pathological lumen expansion in venous malformation

This study shows that TIE2-mutant endothelial cells overexpress Semaphorin 3A and 3F, which repel wild-type endothelial cells and drive pathological lumen expansion in venous malformations.

Hypoxia regulate developmental coronary angiogenesis potentially through VEGFR2- and SOX17-mediated signaling

The paper investigates how hypoxia affects coronary vessel development in mouse hearts and identifies VEGF-R2- and SOX17-mediated signaling as potential downstream pathways.