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Negative Regulation of Soluble Flt-1 and Soluble Endoglin Release by Heme Oxygenase-1
Author(s) -
Melissa Cudmore,
Shakil Ahmad,
Bahjat AlAni,
Takeshi Fujisawa,
Heather Coxall,
Kunal Chudasama,
Luke Devey,
Stephen J. Wigmore,
Allyah Abbas,
Peter W. Hewett,
Asif Ahmed
Publication year - 2007
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.106.660134
Subject(s) - preeclampsia , heme oxygenase , medicine , downregulation and upregulation , placental growth factor , endoglin , endocrinology , vascular endothelial growth factor , endothelial dysfunction , heme , pharmacology , chemistry , biology , vegf receptors , microbiology and biotechnology , biochemistry , pregnancy , genetics , stem cell , gene , cd34 , enzyme
Preeclampsia is characterized clinically by hypertension and proteinuria. Soluble Flt-1 (sFlt-1; also known as soluble vascular endothelial growth factor receptor-1 [VEGFR-1]) and soluble endoglin (sEng) are elevated in preeclampsia, and their administration to pregnant rats elicits preeclampsia-like symptoms. Heme oxygenase-1 (HO-1) and its metabolite carbon monoxide (CO) exert protective effects against oxidative stimuli. Thus, we hypothesized that HO-1 upregulation may offer protection against preeclampsia by inhibiting sFlt-1 and sEng release.

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