Abstract
Urokinase plasminogen activator receptor (uPAR) is a multifaceted, GPI-anchored three-domain protein. Release of the receptor results in variable levels of soluble uPAR (suPAR) in the blood circulation. suPAR levels have been linked to many disease states. In this mini-review, we discuss suPAR as a key circulating molecule mediating kidney disease with a particular focus on differently spliced isoforms.
Highlights
Urokinase plasminogen activator receptor is a multifaceted, GPI-anchored three-domain protein
The urokinase-type plasminogen activator receptor is a GPI-anchored membrane bound protein involved in many physiological and pathological events. It acts as a receptor for urokinasetype plasminogen activator, facilitating the generation of activated plasmin, playing a role in the directional invasion of migrating cells. It is implicated in a plethora of cellular responses that include cellular adhesion, differentiation, proliferation and migration in a nonproteolytic fashion as a signaling orchestrator [1, 2]. Urokinase plasminogen activator receptor (uPAR) is a member of the lymphocyte antigen 6 (Ly-6) superfamily proteins, containing three domains, namely DI-DIII, as numbered from the N terminus [3]
We found the induction of glomerular uPAR in both human and rodent proteinuric kidney diseases
Summary
The urokinase-type plasminogen activator receptor (uPAR) is a GPI-anchored membrane bound protein involved in many physiological and pathological events. It acts as a receptor for urokinasetype plasminogen activator (uPA), facilitating the generation of activated plasmin, playing a role in the directional invasion of migrating cells. Protein structure analyses show that uPAR packs into a concave structure with uPA binding to the central cleft, while vitronectin binding to the outside surface [4, 5]. An unusual implication of uPAR in obstructive nephropathy was reported in unilateral ureteral obstruction (UUO) mouse model, whereby uPAR deficiency accelerated renal fibrosis [18, 19] These findings suggest that renal uPAR may have protective effects in attenuating the fibrogenic response to some renal injury. UPAR activated αVβ3 integrin in podocytes, promoting cell motility and the activation of small GTPase Rac-1 [21]
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