LRG1 Alters Pericyte Phenotype and Compromises Vascular Maturation

Upregulation of leucine-rich alpha-2-glycoprotein-1 (LRG1) contributes to aberrant neovascularization in many different diseases. In contrast, LRG1 is not involved in developmental angiogenesis. Here, we investigated the vasculopathic properties of LRG1 by examining its effect on developing retinal blood vessels. By injecting recombinant protein or an expression vector into the mouse retina during vascular development, we showed that exogenous LRG1 reduces pericyte coverage and NG2 expression. It leads to diminished collagen IV sheathing, fewer adhesion and gap junctions, and reduced vessel calibre and vascular density. Moreover, in mouse retinae containing exogenous LRG1, the developing blood-retinal barrier remains more permeable with significantly higher numbers of transcytotic vesicles present in microvascular endothelial cells. These results reveal that exogeneous LRG1 is sufficient to interfere with the maturation of developing retinal vessels and drive vessel development towards a dysfunctional phenotype. These observations deliver further evidence that LRG1 is an angiopathic factor and highlight the therapeutic potential of blocking LRG1 in diseases characterized by pathogenic angiogenesis or vascular remodelling.

Authors

Institutions

Publication Details

Journal
Cells
Published
2025-04-14
DOI
https://doi.org/10.3390/cells14080593
Primary Topic
Clusterin in disease pathology
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

LRG1 Alters Pericyte Phenotype and Compromises Vascular Maturation

Alexandra E. Hoeh, Mark Basche, Giulia De Rossi, Alessandro Fantin et al.
1 links
Cells
Clusterin in disease pathology
article

LRG1 Alters Pericyte Phenotype and Compromises Vascular Maturation

Alexandra E. Hoeh, Mark Basche, Giulia De Rossi, Alessandro Fantin, Anastasios Sepetis, Patric Turowski, John Greenwood, Stephen E. Moss, Athina Dritsoula, Robin R. Ali, Jui-Hsien Chang, Robert A. Mueller
article en

Abstract

Upregulation of leucine-rich alpha-2-glycoprotein-1 (LRG1) contributes to aberrant neovascularization in many different diseases. In contrast, LRG1 is not involved in developmental angiogenesis. Here, we investigated the vasculopathic properties of LRG1 by examining its effect on developing retinal blood vessels. By injecting recombinant protein or an expression vector into the mouse retina during vascular development, we showed that exogenous LRG1 reduces pericyte coverage and NG2 expression. It leads to diminished collagen IV sheathing, fewer adhesion and gap junctions, and reduced vessel calibre and vascular density. Moreover, in mouse retinae containing exogenous LRG1, the developing blood-retinal barrier remains more permeable with significantly higher numbers of transcytotic vesicles present in microvascular endothelial cells. These results reveal that exogeneous LRG1 is sufficient to interfere with the maturation of developing retinal vessels and drive vessel development towards a dysfunctional phenotype. These observations deliver further evidence that LRG1 is an angiopathic factor and highlight the therapeutic potential of blocking LRG1 in diseases characterized by pathogenic angiogenesis or vascular remodelling.

CellsVol. 14(8)
King's College London (GB), University of Milan (IT), Cell and Gene Therapy Catapult (GB), University College London (GB)
Wellcome, British Heart Foundation, Diabetes UK, Deutsche Forschungsgemeinschaft, Moorfields Eye Charity
Good health and well-being
Openalex Percentile: Top 89%
Clusterin in disease pathology
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.