2022
DOI: 10.1002/path.5969
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Glomerular basement membrane deposition of collagen α1(III) in Alport glomeruli by mesangial filopodia injures podocytes via aberrant signaling through DDR1 and integrin α2β1

Abstract: In Alport mice, activation of the endothelin A receptor (ETAR) in mesangial cells results in sub‐endothelial invasion of glomerular capillaries by mesangial filopodia. Filopodia deposit mesangial matrix in the glomerular basement membrane (GBM), including laminin 211 which activates NF‐κB, resulting in induction of inflammatory cytokines. Herein we show that collagen α1(III) is also deposited in the GBM. Collagen α1(III) localized to the mesangium in wild‐type mice and was found in both the mesangium and the G… Show more

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“…The second, which for the moment is hypothetical, is that the absence of the type IV collagen α3/α4/α5 network may change cell signaling in podocytes via direct interaction of the type IV collagen α1/α2 network with podocytes [6]. Recent evidence has emerged that shows that collagen α1/α2 in Alport glomeruli does not activate the collagen receptor DDR1, suggesting that this network does not contact the DDR1 receptors at the interface between podocyte pedicles and the GBM [7].…”
Section: Introductionmentioning
confidence: 99%
“…The second, which for the moment is hypothetical, is that the absence of the type IV collagen α3/α4/α5 network may change cell signaling in podocytes via direct interaction of the type IV collagen α1/α2 network with podocytes [6]. Recent evidence has emerged that shows that collagen α1/α2 in Alport glomeruli does not activate the collagen receptor DDR1, suggesting that this network does not contact the DDR1 receptors at the interface between podocyte pedicles and the GBM [7].…”
Section: Introductionmentioning
confidence: 99%