This study investigates the role of protease-activated receptor 1 (PAR-1) in podocyte injury leading to focal segmental glomerulosclerosis (FSGS). Using transgenic mice with podocyte-specific expression of constitutively active PAR-1, researchers demonstrate that PAR-1 activation induces signaling pathways involving JNK, VASP, and Paxillin, resulting in podocyte injury, proteinuria, and glomerulosclerosis. The study also identifies TRPC6 as a modulator of PAR-1 signaling, where its Knockout ameliorates disease progression.
Constitutive activation of PAR-1 in podocytes leads to FSGS-like pathology, including proteinuria and glomerulosclerosis. TRPC6 Knockout in this model reduces proteinuria and extends survival, highlighting its role in PAR-1 mediated signaling.
NPHS2-Cre PAR-1 Active(+/−) transgenic mouse model developed by genOway, featuring podocyte-specific expression of constitutively active PAR-1 to study its role in glomerular disease.
Nephrotic syndrome, Focal segmental glomerulosclerosis, Podocyte injury, PAR-1 signaling, TRPC6 modulation
Transgenic model with podocyte-specific expression, NPHS2-Cre driver, Constitutively active PAR-1, TRPC6 Knockout, Glomerular disease modeling
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
