The placenta in toxemia of pregnancy

Tenney, Benjamin; Parker, Frederick B.

doi:10.1016/s0002-9378(40)90458-6

Cited by 142 publications

(41 citation statements)

References 4 publications

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“…Increased syncytial knotting is also referred to as Tenny-Parker change [21] who emphasized that increased budding of placental syncytium is characteristic of preeclapsia [Table/ Fig-6]. When > 30% of tertiary villi possess syncytial buds especially in premature placenta it is diagnostic of a perfusional compromise.…”

Section: Discussionmentioning

confidence: 99%

Foetal Autopsy-Categories and Causes of Death

Fatima

Sherwani

Khan

et al. 2014

JCDR

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Section: Discussionmentioning

confidence: 99%

Foetal Autopsy-Categories and Causes of Death

Fatima

Sherwani

Khan

et al. 2014

JCDR

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“…Here, we identified syncytial knots as the major source of local and circulating sFlt1-14. The fact that these structures increase in number in the normal aging placenta but are much more abundant in the degenerating PE placenta, a phenomenon known as the "Tenney-Parker change," 15 may explain findings that serum levels of soluble receptors (now identified as mostly sFlt1-14) increase in the second and third trimesters of normal pregnancies but to dramatically higher levels in PE pregnancies. These findings place syncytial knotting, a phenomenon common to several placental pathologies, as central to PE pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

A Novel Human-Specific Soluble Vascular Endothelial Growth Factor Receptor 1

Sela

Itin

Natanson-Yaron

et al. 2008

Circulation Research

182

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Abstract-A human-specific splicing variant of vascular endothelial growth factor (VEGF) receptor 1 (Flt1) was discovered, producing a soluble receptor (designated sFlt1-14) that is qualitatively different from the previously described soluble receptor (sFlt1) and functioning as a potent VEGF inhibitor. sFlt1-14 is generated in a cell type-specific fashion, primarily in nonendothelial cells. Notably, in vascular smooth muscle cells, all Flt1 messenger RNA is converted to sFlt1-14, whereas endothelial cells of the same human vessel express sFlt1. sFlt1-14 expression by vascular smooth muscle cells is dynamically regulated as evidenced by its upregulation on coculture with endothelial cells or by direct exposure to VEGF. Increased production of soluble VEGF receptors during pregnancy is entirely attributable to induced expression of placental sFlt1-14 starting by the end of the first trimester. Expression is dramatically elevated in the placenta of women with preeclampsia, specifically induced in abnormal clusters of degenerative syncytiotrophoblasts known as syncytial knots, where it may undergo further messenger RNA editing. sFlt1-14 is the predominant VEGF-inhibiting protein produced by the preeclamptic placenta, accumulates in the circulation, and hence is capable of neutralizing VEGF in distant organs affected in preeclampsia. Together, these findings revealed a new natural VEGF inhibitor that has evolved in humans, possibly to protect nonendothelial cells from adverse VEGF signaling. Furthermore, the study uncovered the identity of a VEGF-blocking protein implicated in preeclampsia. Key Words: VEGF Ⅲ soluble VEGF receptor Ⅲ splicing Ⅲ preeclampsia Ⅲ vascular smooth muscle cell V ascular endothelial growth factor (VEGF) is the key factor promoting vasculogenesis and angiogenesis in the embryo and the factor orchestrating most, if not all, processes of adult neovascularization. In addition, VEGF performs nonvascular developmental functions and plays a number of homeostatic roles in the adult. The latter includes maintenance of endothelial fenestrations, a role in vasodilatation, and neurogenic and neurotrophic activities, among others. 1,2 Not surprisingly, therefore, VEGF is under a tight spatial and temporal regulation, and even a moderate deviation from its exquisite dosage control or perturbation of its precise morphogenetic gradients is detrimental for proper development and organ homeostasis. 3,4 Among the multiple layers of VEGF control, natural VEGF inhibitors, primarily soluble VEGF receptors, are likely to be important. Indeed, VEGF receptor-1 (Flt1) messenger RNA (mRNA) may undergo alternative splicing in a way that the encoded protein retains the ligand-binding domain but is devoid of the membrane-spanning and intracellular kinase domains, hence functioning as a VEGF-trapping soluble receptor. This secreted protein (designated sFlt1) is a potent inhibitor of both VEGF-A, VEGF-B, and placental growth factor. 2 It is widely used as a research tool for VEGF inhibition and, more recently, also harnessed...

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“…Pregnancies with increased placental mass (e.g., twins, hydrops) and relative reduction of placental perfusion are at increased risk of developing preeclampsia (1)(2)(3)(4). Many investigators postulate that placental ischemia is an initiating event in the pathogenesis of this disease (2,5,6). Accumulating evidence suggests that placental ischemia results in local metabolic changes (7) and the production of circulating factors that alter maternal endothelial function (8).…”

Section: Introductionmentioning

confidence: 99%

Angiotensinogen T235 expression is elevated in decidual spiral arteries.

Morgan¹,

Craven²,

Nelson³

et al. 1997

J. Clin. Invest.

108

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Preeclampsia is associated with a common molecular variant of angiotensinogen (Met235Thr). This variant is in tight linkage disequilibrium with a mutation in the angiotensinogen promoter, G( Ϫ 6)A, which leads to elevated expression in vitro. Since angiotensin II levels could play a role in atherotic changes of the uterine spiral arteries associated with preeclampsia, we investigated angiotensinogen expression in the first trimester uterus. We localized angiotensinogen transcription in uterine decidua using in situ reverse transcription PCR. We then compared decidual T235 expression levels to M235 levels in heterozygous women using an allele-specific ligation assay and a single nucleotide primer extension assay. In human decidua, angiotensinogen is expressed only in spiral artery smooth muscle cells. Heterozygous women have significantly elevated expression of the T235 allele compared to the M235 allele ( P Ͻ 0.0001). These observations suggest that elevated expression of the T235 allele in decidual spiral arteries may cause first trimester atherotic changes leading to preeclampsia. ( J. Clin.

show abstract

The placenta in toxemia of pregnancy

Cited by 142 publications

References 4 publications

Foetal Autopsy-Categories and Causes of Death

Foetal Autopsy-Categories and Causes of Death

A Novel Human-Specific Soluble Vascular Endothelial Growth Factor Receptor 1

Angiotensinogen T235 expression is elevated in decidual spiral arteries.

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