Recovery of Renal Function following Kidney-Specific VEGF Therapy in Experimental Renovascular Disease.


Journal

American journal of nephrology
ISSN: 1421-9670
Titre abrégé: Am J Nephrol
Pays: Switzerland
ID NLM: 8109361

Informations de publication

Date de publication:
2020
Historique:
received: 11 06 2020
accepted: 31 08 2020
pubmed: 2 11 2020
medline: 14 9 2021
entrez: 1 11 2020
Statut: ppublish

Résumé

Chronic renovascular disease (RVD) can lead to a progressive loss of renal function, and current treatments are inefficient. We designed a fusion of vascular endothelial growth factor (VEGF) conjugated to an elastin-like polypeptide (ELP) carrier protein with an N-terminal kidney-targeting peptide (KTP). We tested the hypothesis that KTP-ELP-VEGF therapy will effectively recover renal function with an improved targeting profile. Further, we aimed to elucidate potential mechanisms driving renal recovery. Unilateral RVD was induced in 14 pigs. Six weeks later, renal blood flow (RBF) and glomerular filtration rate (GFR) were quantified by multidetector CT imaging. Pigs then received a single intrarenal injection of KTP-ELP-VEGF or vehicle. CT quantification of renal hemodynamics was repeated 4 weeks later, and then pigs were euthanized. Ex vivo renal microvascular (MV) density and media-to-lumen ratio, macrophage infiltration, and fibrosis were quantified. In parallel, THP-1 human monocytes were differentiated into naïve macrophages (M0) or inflammatory macrophages (M1) and incubated with VEGF, KTP-ELP, KTP-ELP-VEGF, or control media. The mRNA expression of macrophage polarization and angiogenic markers was quantified (qPCR). Intrarenal KTP-ELP-VEGF improved RBF, GFR, and MV density and attenuated MV media-to-lumen ratio and renal fibrosis compared to placebo, accompanied by augmented renal M2 macrophages. In vitro, exposure to VEGF/KTP-ELP-VEGF shifted M0 macrophages to a proangiogenic M2 phenotype while M1s were nonresponsive to VEGF treatment. Our results support the efficacy of a new renal-specific biologic construct in recovering renal function and suggest that VEGF may directly influence macrophage phenotype as a possible mechanism to improve MV integrity and function in the stenotic kidney.

Sections du résumé

BACKGROUND
Chronic renovascular disease (RVD) can lead to a progressive loss of renal function, and current treatments are inefficient. We designed a fusion of vascular endothelial growth factor (VEGF) conjugated to an elastin-like polypeptide (ELP) carrier protein with an N-terminal kidney-targeting peptide (KTP). We tested the hypothesis that KTP-ELP-VEGF therapy will effectively recover renal function with an improved targeting profile. Further, we aimed to elucidate potential mechanisms driving renal recovery.
METHODS
Unilateral RVD was induced in 14 pigs. Six weeks later, renal blood flow (RBF) and glomerular filtration rate (GFR) were quantified by multidetector CT imaging. Pigs then received a single intrarenal injection of KTP-ELP-VEGF or vehicle. CT quantification of renal hemodynamics was repeated 4 weeks later, and then pigs were euthanized. Ex vivo renal microvascular (MV) density and media-to-lumen ratio, macrophage infiltration, and fibrosis were quantified. In parallel, THP-1 human monocytes were differentiated into naïve macrophages (M0) or inflammatory macrophages (M1) and incubated with VEGF, KTP-ELP, KTP-ELP-VEGF, or control media. The mRNA expression of macrophage polarization and angiogenic markers was quantified (qPCR).
RESULTS
Intrarenal KTP-ELP-VEGF improved RBF, GFR, and MV density and attenuated MV media-to-lumen ratio and renal fibrosis compared to placebo, accompanied by augmented renal M2 macrophages. In vitro, exposure to VEGF/KTP-ELP-VEGF shifted M0 macrophages to a proangiogenic M2 phenotype while M1s were nonresponsive to VEGF treatment.
CONCLUSIONS
Our results support the efficacy of a new renal-specific biologic construct in recovering renal function and suggest that VEGF may directly influence macrophage phenotype as a possible mechanism to improve MV integrity and function in the stenotic kidney.

Identifiants

pubmed: 33130676
pii: 000511260
doi: 10.1159/000511260
pmc: PMC7750286
mid: NIHMS1633333
doi:

Substances chimiques

Peptides 0
Recombinant Fusion Proteins 0
VEGFA protein, human 0
Vascular Endothelial Growth Factor A 0
Elastin 9007-58-3

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

891-902

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL051971
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM104357
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL095638
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL121527
Pays : United States

Informations de copyright

© 2020 S. Karger AG, Basel.

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Auteurs

Jason E Engel (JE)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Maxx L Williams (ML)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Erika Williams (E)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Camille Azar (C)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Erin B Taylor (EB)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Gene L Bidwell (GL)

Department of Neurology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Alejandro R Chade (AR)

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA, achade@umc.edu.
Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA, achade@umc.edu.
Department of Radiology, University of Mississippi Medical Center, Jackson, Mississippi, USA, achade@umc.edu.

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