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Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases

Vera Eremina, Manish Sood, Jody Haigh, András Nagy, Ginette Lajoie, Napoleone Ferrara, Hans-Peter Gerber, Yamato Kikkawa, Jeffrey H Miner and Susan E Quaggin (2003) JOURNAL OF CLINICAL INVESTIGATION. 111(5). p.707-716
abstract
Kidney disease affects over 20 million people in the United States alone. Although the causes of renal failure are diverse, the glomerular filtration barrier is often the target of injury. Dysregulation of VEGF expression within the glomerulus has been demonstrated in a wide range of primary and acquired renal diseases, although the significance of these changes is unknown. in the glomerulus, VEGF-A is highly expressed in podocytes that make up a major portion of the barrier between the blood and urinary spaces. in this paper, we show that glomerular-selective deletion or overexpression of VEGF-A leads to glomerular disease in mice. Podocyte-specific heterozygosity for VEGF-A resulted in renal disease by 2.5 weeks of age, characterized by proteinuria and endotheliosis, the renal lesion seen in preeclampsia. Homozygous deletion of VEGF-A in glomeruli resulted in perinatal lethality. Mutant kidneys failed to develop a filtration barrier due to defects in endothelial cell migration, differentiation, and survival. In contrast, podocyte-specific overexpression of the VEGF-164 isoform led to a striking collapsing glomerulopathy, the lesion seen in HIV-associated nephropathy. Our data demonstrate that tight regulation of VEGF-A signaling is critical for establishment and maintenance of the glomerular filtration barrier and strongly supports a pivotal role for VEGF-A in renal disease.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
ENDOTHELIAL GROWTH-FACTOR, FOCAL SEGMENTAL GLOMERULOSCLEROSIS, KAPOSIS-SARCOMA CELLS, HIV-ASSOCIATED NEPHROPATHY, TAT, PODOCYTE, KIDNEY, GENE, GLOMERULOGENESIS, MICE
journal title
JOURNAL OF CLINICAL INVESTIGATION
J. Clin. Invest.
volume
111
issue
5
pages
707 - 716
Web of Science type
Article
Web of Science id
000181346600019
JCR category
MEDICINE, RESEARCH & EXPERIMENTAL
JCR impact factor
14.307 (2003)
JCR rank
3/72 (2003)
JCR quartile
1 (2003)
ISSN
0021-9738
DOI
10.1172/JCI200317423
language
English
UGent publication?
no
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1202150
handle
http://hdl.handle.net/1854/LU-1202150
date created
2011-04-05 11:47:04
date last changed
2017-04-07 12:15:28
@article{1202150,
  abstract     = {Kidney disease affects over 20 million people in the United States alone. Although the causes of renal failure are diverse, the glomerular filtration barrier is often the target of injury. Dysregulation of VEGF expression within the glomerulus has been demonstrated in a wide range of primary and acquired renal diseases, although the significance of these changes is unknown. in the glomerulus, VEGF-A is highly expressed in podocytes that make up a major portion of the barrier between the blood and urinary spaces. in this paper, we show that glomerular-selective deletion or overexpression of VEGF-A leads to glomerular disease in mice. Podocyte-specific heterozygosity for VEGF-A resulted in renal disease by 2.5 weeks of age, characterized by proteinuria and endotheliosis, the renal lesion seen in preeclampsia. Homozygous deletion of VEGF-A in glomeruli resulted in perinatal lethality. Mutant kidneys failed to develop a filtration barrier due to defects in endothelial cell migration, differentiation, and survival. In contrast, podocyte-specific overexpression of the VEGF-164 isoform led to a striking collapsing glomerulopathy, the lesion seen in HIV-associated nephropathy. Our data demonstrate that tight regulation of VEGF-A signaling is critical for establishment and maintenance of the glomerular filtration barrier and strongly supports a pivotal role for VEGF-A in renal disease.},
  author       = {Eremina, Vera and Sood, Manish and Haigh, Jody and Nagy, Andr{\'a}s and Lajoie, Ginette and Ferrara, Napoleone and Gerber, Hans-Peter and Kikkawa, Yamato and Miner, Jeffrey H and Quaggin, Susan E},
  issn         = {0021-9738},
  journal      = {JOURNAL OF CLINICAL INVESTIGATION},
  keyword      = {ENDOTHELIAL GROWTH-FACTOR,FOCAL SEGMENTAL GLOMERULOSCLEROSIS,KAPOSIS-SARCOMA CELLS,HIV-ASSOCIATED NEPHROPATHY,TAT,PODOCYTE,KIDNEY,GENE,GLOMERULOGENESIS,MICE},
  language     = {eng},
  number       = {5},
  pages        = {707--716},
  title        = {Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases},
  url          = {http://dx.doi.org/10.1172/JCI200317423},
  volume       = {111},
  year         = {2003},
}

Chicago
Eremina, Vera, Manish Sood, Jody Haigh, András Nagy, Ginette Lajoie, Napoleone Ferrara, Hans-Peter Gerber, Yamato Kikkawa, Jeffrey H Miner, and Susan E Quaggin. 2003. “Glomerular-specific Alterations of VEGF-A Expression Lead to Distinct Congenital and Acquired Renal Diseases.” Journal of Clinical Investigation 111 (5): 707–716.
APA
Eremina, V., Sood, M., Haigh, J., Nagy, A., Lajoie, G., Ferrara, N., Gerber, H.-P., et al. (2003). Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. JOURNAL OF CLINICAL INVESTIGATION, 111(5), 707–716.
Vancouver
1.
Eremina V, Sood M, Haigh J, Nagy A, Lajoie G, Ferrara N, et al. Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. JOURNAL OF CLINICAL INVESTIGATION. 2003;111(5):707–16.
MLA
Eremina, Vera, Manish Sood, Jody Haigh, et al. “Glomerular-specific Alterations of VEGF-A Expression Lead to Distinct Congenital and Acquired Renal Diseases.” JOURNAL OF CLINICAL INVESTIGATION 111.5 (2003): 707–716. Print.