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Soluble endoglin contributes to the pathogenesis of preeclampsia
TLDR
A novel placenta-derived soluble TGF-β coreceptor, endoglin (sEng), which is elevated in the sera of preeclamptic individuals, correlates with disease severity and falls after delivery, suggest that sEng may act in concert with sFlt1 to induce severe preeclampsia. Expand
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
TLDR
It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia. Expand
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia.
TLDR
It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia. Expand
Circulating angiogenic factors and the risk of preeclampsia*
TLDR
Alterations in the levels of sFlt-1 and free PlGF were greater in women with an earlier onset of preeclampsia and in women in whom preeClampsia was associated with a small-for-gestational-age infant. Expand
Co-assembly of polycystin-1 and -2 produces unique cation-permeable currents
TLDR
Polycystin-1 and -2 co-assemble at the plasma membrane to produce a new channel and to regulate renal tubular morphology and function, and are shown to interact to produce new calcium-permeable non-selective cation currents. Expand
Homo- and heterodimeric interactions between the gene products of PKD1 and PKD2.
TLDR
PKD1 and PKD2 may function through a common signaling pathway that is necessary for normal tubulogenesis and that PKD1 may require the presence of PKD 2 for stable expression. Expand
Excess Circulating Angiopoietin-2 May Contribute to Pulmonary Vascular Leak in Sepsis in Humans
TLDR
A critical role is identified in disrupting normal pulmonary endothelial function in sepsis-associated lung injury and excess systemic Ang-2 provokes pulmonary leak and congestion in otherwise healthy adult mice. Expand
A zinc finger-encoding gene coregulated with c-fos during growth and differentiation, and after cellular depolarization
TLDR
Sequence analysis of murine Egr-1 cDNA predicts a protein with three DNA binding zinc fingers, and results suggest that EGR1 may function as a transcriptional regulator in diverse biological processes. Expand
Hypoxic induction of human vascular endothelial growth factor expression through c-Src activation
TLDR
The results provide an insight into hypoxia-triggered intracellular signalling, define VEGF as a new downstream target for c-Src, and suggest a role for c -Src in promoting angiogenesis. Expand
Hemodialysis vascular access dysfunction: a cellular and molecular viewpoint.
TLDR
There have been inadequate efforts by the nephrology community to translate the recent advances in molecular and interventional cardiology into therapies for hemodialysis vascular access, and some broad guidelines for future innovative translational and clinical research in this area are offered. Expand
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