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Related Experiment Video

Updated: May 5, 2026

A Revised Method for Inducing Secondary Lymphedema in the Hindlimb of Mice

A Revised Method for Inducing Secondary Lymphedema in the Hindlimb of Mice

Published on: November 2, 2019

Targeting uPARAP Modifies Lymphatic Vessel Architecture and Attenuates Lymphedema.

Fabrice Gucciardo¹, Alizée Lebeau¹, Sébastien Pirson¹

¹From the Laboratory of Tumor and Development Biology, GIGA (F.G., A.L., S.P., F.B., E.I., S.B., J.D., L.B., A.P., C.M., M.G.-I., A.N.), University of Liège, Sart-Tilman, Belgium.

|March 4, 2025

Summary

Targeting uPARAP (urokinase plasminogen activator receptor-associated protein) can attenuate lymphedema by remodeling lymphatic vasculature. This approach offers a novel therapeutic strategy for lymphedema by improving fluid absorption.

Keywords:

adherens junctions cadherins lymphatic vessels lymphedema

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Last Updated: May 5, 2026

A Revised Method for Inducing Secondary Lymphedema in the Hindlimb of Mice

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Published on: May 14, 2020

A Murine Tail Lymphedema Model

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Published on: February 10, 2021

Area of Science:

Vascular Biology
Lymphatic Research
Fibrosis Mechanisms

Background:

Lymphedema is a chronic condition characterized by lymphatic dysfunction, leading to tissue swelling and fibrosis.
Current treatments for lymphedema are limited, highlighting the need for novel therapeutic strategies.

Purpose of the Study:

To investigate the role of uPARAP (urokinase plasminogen activator receptor-associated protein) in lymphedema pathogenesis.
To determine if interfering with uPARAP can attenuate lymphedema by modulating lymphatic vasculature.

Main Methods:

Generated mice with specific uPARAP deficiency in lymphatic endothelial cells (LECs).
Utilized a preclinical model of secondary lymphedema (SL) for analysis.
Assessed cellular effects of uPARAP deletion on lymphatic permeability in vitro and in vivo.
Investigated uPARAP interactions with cell junction proteins and employed computational modeling.

Main Results:

uPARAP deficiency mitigated key lymphedema features, including swelling and epidermal thickening.
Absence of uPARAP led to a distinctive labyrinthine lymphatic vasculature with improved fluid-absorbing capacity.
uPARAP knockdown impaired vascular endothelial growth factor C-mediated trafficking and induced overlapping cell junctions in LECs.
Pharmacologic inhibition of ROCK mimicked these effects and attenuated SL.

Conclusions:

Downregulating uPARAP induces beneficial lymphatic vasculature remodeling, attenuating lymphedema.
This remodeling occurs via a cell junction-based mechanism, offering a novel therapeutic pathway.
Targeting uPARAP with a gapmer approach demonstrates therapeutic potential for lymphedema treatment.