Inhibiting The uPA/uPAR Pathway Affords Photoreceptor Resilience and Preserves Retinal Function in a Mouse Model of Retinitis Pigmentosa.

ABSTRACT:

Purpose

Retinitis pigmentosa (RP) is characterized by primary rod degeneration followed by secondary cone death. The urokinase-type plasminogen activator (uPA) and its cognate receptor (uPAR) have been recently suggested to regulate pro-inflammatory events in RP possibly through the interaction of uPAR with its lateral partners, including formyl peptide receptors (FPRs). This study explored whether the inhibition of the crosstalk between uPAR and FPR1 may counteract photoreceptor degeneration in the rd10 mouse model of RP.

Methods

The newly synthetized FPR1 antagonist N-19004 was subcutaneously administered to rd10 mice from post-natal day (PD) 10 to PD 30. The efficacy of N-19004 on retinal function and morphology was evaluated by electroretinogram (ERG) and optical coheren

SUBMITTER: Amato R 

PROVIDER: S-EPMC12364010 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature