Apelin-VEGF-C mRNA delivery as therapeutic for the treatment of secondary lymphedema.
Justine CreffAsalaa LamaaEmeline BenuzziElisa BalzanFrancoise PujolTangra Draia-NicolauManon NouguéLena VerduFlorent MorfoisseEric LacazettePhilippe ValetBenoit ChaputFabian GrossRegis GayonPascale BouilléJulie Malloizel-DelaunayAlessandra Bura RivièreAnne-Catherine PratsBarbara Garmy-SusiniPublished in: EMBO molecular medicine (2024)
Secondary lymphedema (LD) corresponds to a severe lymphatic dysfunction leading to the accumulation of fluid and fibrotic adipose tissue in a limb. Here, we identified apelin (APLN) as a powerful molecule for regenerating lymphatic function in LD. We identified the loss of APLN expression in the lymphedematous arm compared to the normal arm in patients. The role of APLN in LD was confirmed in APLN knockout mice, in which LD is increased and associated with fibrosis and dermal backflow. This was reversed by intradermal injection of APLN-lentivectors. Mechanistically, APLN stimulates lymphatic endothelial cell gene expression and induces the binding of E2F8 transcription factor to the promoter of CCBE1 that controls VEGF-C processing. In addition, APLN induces Akt and eNOS pathways to stimulate lymphatic collector pumping. Our results show that APLN represents a novel partner for VEGF-C to restore lymphatic function in both initial and collecting vessels. As LD appears after cancer treatment, we validated the APLN-VEGF-C combination using a novel class of nonintegrative RNA delivery LentiFlash® vector that will be evaluated for phase I/IIa clinical trial.
Keyphrases
- endothelial cells
- lymph node
- gene expression
- vascular endothelial growth factor
- transcription factor
- adipose tissue
- clinical trial
- end stage renal disease
- dna methylation
- poor prognosis
- oxidative stress
- chronic kidney disease
- signaling pathway
- newly diagnosed
- binding protein
- peritoneal dialysis
- high glucose
- high fat diet
- early onset
- cell proliferation
- skeletal muscle
- patient reported outcomes
- metabolic syndrome
- phase ii
- open label
- nucleic acid
- phase iii