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The role of PDGF-D in mesangioproliferative glomerulonephritis
Jürgen Floege1, Claudia van Roeyen, Peter Boor
1Division of Nephrology and Immunology, RWTH University of Aachen, Aachen, Germany. Juergen.Floege@rwth-aachen.de
Insights
Platelet-derived growth factor D (PDGF-D) drives mesangioproliferative nephritis, a key factor in kidney disease. Targeting PDGF-D offers a promising therapeutic strategy for end-stage renal disease (ESRD).
Area of Science:
- Nephrology
- Molecular Biology
- Pathology
Background:
- End-stage renal disease (ESRD) is increasing, necessitating new treatments for underlying conditions like mesangioproliferative glomerulonephritis.
- Platelet-derived growth factor (PDGF) B chain's role in mesangioproliferative changes is known, but PDGF-D's role is emerging.
- PDGF-D signals via the PDGF beta-receptor, sharing functions with PDGF-B.
Purpose of the Study:
- To investigate the role of PDGF-D in mesangioproliferative nephritis.
- To explore PDGF-D as a potential therapeutic target for kidney diseases.
Main Methods:
- In vitro studies assessing PDGF-D's effect on mesangial cell proliferation.
- In vivo studies using adenoviral vectors to express PDGF-D in mice.
- In vivo studies using PDGF-D antagonism in a rat model of mesangioproliferative disease.
Main Results:
- PDGF-D induces mesangial cell proliferation in vitro.
- PDGF-D is overexpressed in human mesangioproliferative glomerulonephritis.
- Hepatic PDGF-D expression caused nephritis in mice; PDGF-D antagonism improved renal changes in rats.
- PDGF-D may also contribute to tubulointerstitial fibrosis in progressive renal failure.
Conclusions:
- PDGF-D is a significant mediator of mesangioproliferative nephritis, similar to PDGF-B.
- PDGF-D represents a potential therapeutic target for mesangioproliferative nephritis and possibly progressive renal failure.
- Further research into PDGF-D's role in renal pathology is warranted.
Abstract:
In view of increasing numbers of patients with end-stage renal disease (ESRD), new approaches to common underlying diseases, such as mesangioproliferative glomerulonephritis, including IgA nephropathy, are urgently needed. Whereas the role of the platelet-derived growth factor (PDGF) B chain in mediating mesangioproliferative changes is well established, the role of the PDGF-D chain has only recently been elucidated. The PDGF-D chain, like PDGF-B, signals through the PDGF beta-receptor and therefore shares a number of biological activities with PDGF-B. Recent studies have shown that PDGF-D induces mesangial cell proliferation in vitro and is overexpressed in mesangioproliferative glomerulonephritis in vivo. Hepatic transfection with an adenoviral vector expressing PDGF-D induced prominent mesangioproliferative nephritis in mice, whereas antagonism of PDGF-D in a rat model of mesangioproliferative disease ameliorated the renal changes. These four observations establish PDGF-D, like -B, as an important mediator of mesangioproliferative nephritis in vivo and suggest that it may be an attractive therapeutic target. In addition, first observations suggest that PDGF-D may also contribute to secondary renal changes that characterize progressive renal failure, i.e. tubulointerstitial fibrosis.
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