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PP038. Renal ETK/BMX activation decreased in preeclampsia

Strevens, Helena LU ; Wide-Swensson, Dag LU ; Hansson, Ola LU orcid and Melander, Olle LU orcid (2013) In Pregnancy Hypertension 3(2). p.80-80
Abstract

INTRODUCTION: Vascular endothelial growth factors (VEGF's) are essential to angiogenesis and play a central role in the pathophysiology of preeclampsia. Specifically, antagonists of VEGFR2 cause a preeclampsia-like syndrome, in humans and rats[1]. ETK/BMX is a receptor tyrosine kinase (RTK) which induces VEGF expression and forms a complex with VEGFR2, whereby VEGF and TNF can induce a reciprocal activation of both kinases.

OBJECTIVES: To determine the levels of phosphorylation, and thus activation, of VEGFR2 and ETK/BMX in renal tissue from women with preeclampsia and with healthy pregnancies.

METHODS: Renal tissue was obtained with consent from six preeclamptic and six healthy pregnant women included in a previous renal... (More)

INTRODUCTION: Vascular endothelial growth factors (VEGF's) are essential to angiogenesis and play a central role in the pathophysiology of preeclampsia. Specifically, antagonists of VEGFR2 cause a preeclampsia-like syndrome, in humans and rats[1]. ETK/BMX is a receptor tyrosine kinase (RTK) which induces VEGF expression and forms a complex with VEGFR2, whereby VEGF and TNF can induce a reciprocal activation of both kinases.

OBJECTIVES: To determine the levels of phosphorylation, and thus activation, of VEGFR2 and ETK/BMX in renal tissue from women with preeclampsia and with healthy pregnancies.

METHODS: Renal tissue was obtained with consent from six preeclamptic and six healthy pregnant women included in a previous renal needle biopsy study[2] and a RayBio® Phosphorylation Antibody Array was used according to instructions.

RESULTS: Phosphorylated ETK/BMX was significantly reduced in the preeclamptic women compared to in the healthy pregnant women. There was no difference in phosphorylated VEGFR2 between groups.

CONCLUSION: These data suggest that ETK/BMX could be an important mediator of VEGF function in healthy pregnancy, in the kidneys more so than VEGFR2, and that absence of the positive feedforward signalling that ETK/BMX and VEGF together accomplish, and/or a TNF induced activation of this, may play a role in the pathophysiology of preeclampsia.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pregnancy Hypertension
volume
3
issue
2
pages
80 - 80
publisher
Elsevier
external identifiers
  • pmid:26105894
ISSN
2210-7789
DOI
10.1016/j.preghy.2013.04.065
language
English
LU publication?
yes
additional info
Copyright © 2013. Published by Elsevier B.V.
id
43826800-7b0e-45e9-9797-7694d69470cf
date added to LUP
2020-11-24 08:45:32
date last changed
2020-11-25 02:20:56
@article{43826800-7b0e-45e9-9797-7694d69470cf,
  abstract     = {{<p>INTRODUCTION: Vascular endothelial growth factors (VEGF's) are essential to angiogenesis and play a central role in the pathophysiology of preeclampsia. Specifically, antagonists of VEGFR2 cause a preeclampsia-like syndrome, in humans and rats[1]. ETK/BMX is a receptor tyrosine kinase (RTK) which induces VEGF expression and forms a complex with VEGFR2, whereby VEGF and TNF can induce a reciprocal activation of both kinases.</p><p>OBJECTIVES: To determine the levels of phosphorylation, and thus activation, of VEGFR2 and ETK/BMX in renal tissue from women with preeclampsia and with healthy pregnancies.</p><p>METHODS: Renal tissue was obtained with consent from six preeclamptic and six healthy pregnant women included in a previous renal needle biopsy study[2] and a RayBio® Phosphorylation Antibody Array was used according to instructions.</p><p>RESULTS: Phosphorylated ETK/BMX was significantly reduced in the preeclamptic women compared to in the healthy pregnant women. There was no difference in phosphorylated VEGFR2 between groups.</p><p>CONCLUSION: These data suggest that ETK/BMX could be an important mediator of VEGF function in healthy pregnancy, in the kidneys more so than VEGFR2, and that absence of the positive feedforward signalling that ETK/BMX and VEGF together accomplish, and/or a TNF induced activation of this, may play a role in the pathophysiology of preeclampsia.</p>}},
  author       = {{Strevens, Helena and Wide-Swensson, Dag and Hansson, Ola and Melander, Olle}},
  issn         = {{2210-7789}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{80--80}},
  publisher    = {{Elsevier}},
  series       = {{Pregnancy Hypertension}},
  title        = {{PP038. Renal ETK/BMX activation decreased in preeclampsia}},
  url          = {{http://dx.doi.org/10.1016/j.preghy.2013.04.065}},
  doi          = {{10.1016/j.preghy.2013.04.065}},
  volume       = {{3}},
  year         = {{2013}},
}