PP038. Renal ETK/BMX activation decreased in preeclampsia
(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
- Strevens, Helena LU ; Wide-Swensson, Dag LU ; Hansson, Ola LU and Melander, Olle LU
- organization
- publishing date
- 2013-04
- 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}}, }