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Circulating Bone Morphogenetic Protein 1-3 Isoform Increases Renal Fibrosis (CROSBI ID 176146)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Grgurević, Lovorka ; Maček, Boris ; Healy, D.R. ; Brault, A.L. ; Erjavec, Igor ; Čipčić, Antonio ; Grgurević, Ivica ; Rogić, Dunja ; Galešić, Krešo ; Brkljačić, Jelena et al. Circulating Bone Morphogenetic Protein 1-3 Isoform Increases Renal Fibrosis // Journal of the American Society of Nephrology, 22 (2011), 4; 681-692. doi: 10.1681/ASN.2010070722

Podaci o odgovornosti

Grgurević, Lovorka ; Maček, Boris ; Healy, D.R. ; Brault, A.L. ; Erjavec, Igor ; Čipčić, Antonio ; Grgurević, Ivica ; Rogić, Dunja ; Galešić, Krešo ; Brkljačić, Jelena ; Štern-Padovan, Ranka ; Paralkar, V.M. ; Vukičević, Slobodan

engleski

Circulating Bone Morphogenetic Protein 1-3 Isoform Increases Renal Fibrosis

Bone morphogenetic proteins (BMPs) participate in organ regeneration through autocrine and paracrine actions, but the existence and effects of these proteins in the systemic circulation is unknown. Using liquid chromatography mass spectrometry, we identified BMP6, GDF15, and the BMP1-3 isoform of the Bmp1 gene in plasma samples from healthy volunteers and patients with CKD. We isolated the endogenous BMP1-3 protein and demonstrated that it circulates as an active enzyme, evidenced by its ability to cleave dentin matrix protein-1 in vitro. In rats with CKD, administration of recombinant BMP1-3 increased renal fibrosis and reduced survival. In contrast, administration of a BMP1-3-neutralizing antibody reduced renal fibrosis, preserved renal function, and increased survival. In addition, treating with the neutralizing antibody was associated with low plasma levels of TGF beta 1 and connective tissue growth factor. In HEK293 cells and remnant kidneys, BMP1-3 increased the transcription of collagen type I, TGF beta 1, beta-catenin, and BMP7 via a BMP- and Wnt-independent mechanism that involved signaling through an integrin 01 subunit. The profibrotic effect of BMP1-3 may, in part, be a result of the accompanied decrease in decorin (DCN) expression. Taken together, inhibition of circulating BMP1-3 reduces renal fibrosis, suggesting that this pathway may be a therapeutic target for CKD.

Growth-factor-beta. Extracellular-matrix accumulation. Human embryonic-development. Tgf-beta. Experimental glomerulonephritis. Gene-expression. Decorin. Kidney. Receptor. Metalloproteinases

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Podaci o izdanju

22 (4)

2011.

681-692

objavljeno

1046-6673

10.1681/ASN.2010070722

Povezanost rada

Temeljne medicinske znanosti, Kliničke medicinske znanosti, Farmacija

Poveznice
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