Stereological Investigation of Placental Morphology in Pregnancies Complicated by Pre-eclampsia with and without Intrauterine Growth Restriction

Mayhew, Terry M.; Ohadike, C; Baker, Philip N.; Crocker, Ian; Mitchell, Christopher A.; Ong, Stephen

doi:10.1053/plac.2002.0900

Cited by 252 publications

(178 citation statements)

References 55 publications

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“…The human placenta differs morphologically from that of the mouse but is of the same hemochorial type (24). It is therefore important to note that a reduction in placental volume and surface area of the exchange barrier has been reported in cases of IUGR (25,26), proportionally similar to that found in the P0 placentas here. Although measurements of the harmonic mean thickness of the exchange barrier are not available for the human in IUGR, estimates based on the arithmetic mean thickness indicate that the diffusing capacity is reduced by Ϸ50% in these placentas (26).…”

Section: Resultssupporting

confidence: 79%

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

Sibley

Coan

Ferguson-Smith

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

287

213

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Restricted fetal growth is associated with postnatal mortality and morbidity and may be directly related to alterations in the capacity of the placenta to supply nutrients. We proposed previously that imprinted genes can regulate nutrient supply by the placenta. Here, we tested the hypothesis that the insulin-like growth factor 2 gene (Igf2) transcribed from the placental-specific promoter (P0) regulates the development of the diffusional permeability properties of the mouse placenta. Using mice in which placental-specific Igf2 had been deleted (P0), we measured the transfer in vivo of three inert hydrophilic solutes of increasing size ( 14 C-mannitol, 51 CrEDTA, and 14 C-inulin). At embryonic day 19, placental and fetal weights in P0 conceptuses were reduced to 66% and 76%, respectively, of wild type. In P0 mutants, the permeability⅐surface area product for the tracers at this stage of development was 68% of that of controls; this effect was independent of tracer size. Stereological analysis of histological sections revealed the surface area of the exchange barrier in the labyrinth of the mouse placenta to be reduced and thickness increased in P0 fetuses compared to wild type. As a result, the average theoretical diffusing capacity in P0 knockout placentas was dramatically reduced to 40% of that of wild-type placentas. These data show that placental Igf2 regulates the development of the diffusional exchange characteristics of the mouse placenta. This provides a mechanism for the role of imprinted genes in controlling placental nutrient supply and fetal growth. Altered placental Igf2 could be a cause of idiopathic intrauterine growth restriction in the human.

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Section: Resultssupporting

confidence: 79%

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

Sibley

Coan

Ferguson-Smith

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

287

213

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“…Changes in vessel formation within the human preeclamptic placenta are controversial [15][16][17][18][19][20][21]. In particular in LOPE, stereological studies evidenced no changes [22], while estimation of endothelial markers such as CD31 [18] or CD34 [17] denoted elevated placental angiogenesis compared to normotensive controls.…”

Section: Introductionmentioning

confidence: 99%

Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

Acurio

Herlitz

Troncoso

et al. 2016

Purinergic Signalling

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“…The frequency of these lesions is inversely related to the gestational age in which the hypertensive disorder was diagnosed. The earliest the development of hypertension/preeclampsia the more severe are the vascular lesions 111,112 . Moreover, Kovo et al 113 reported that the presence of fetal growth restriction in women with preeclampsia increases also the frequency of fetal vascular lesions.…”

Section: Preeclampsiamentioning

confidence: 99%

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

Mastrolia

Mazor

Loverro

et al. 2014

Preprint

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View the peer-reviewed version (peerj.com/articles/653), which is the preferred citable publication unless you specifically need to cite this preprint. Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromesObstetrical complications including preeclampsia, fetal growth restriction, preterm labor, preterm prelabor rupture of membranes and fetal demise are all the clinical endpoint of several underlying mechanisms (i.e. infection inflammation, thrombosis, endocrine disorder, immunologic rejection, genetic, and environmental), therefore, they may be regarded as syndromes. Placental vascular pathology and increased thrombin generation were reported in all of these obstetrical syndromes. Moreover, elevated concentrations of thrombin-antithrombin III complexes and changes in the coagulation as well as anticoagulation factors can be detected in the maternal circulation prior to the clinical development of the disease in some of these syndromes. In this review, we will assess the changes in the hemostatic system during normal and complicated pregnancy in maternal blood, maternal-fetal interface and amniotic fluid, and describe the contribution of thrombosis and vascular pathology to the development of the great obstetrical syndromes.PeerJ PrePrints | http://dx.doi.org/10.7287/peerj.preprints.487v1 | CC-BY 4.0 Open Access |

show abstract

Stereological Investigation of Placental Morphology in Pregnancies Complicated by Pre-eclampsia with and without Intrauterine Growth Restriction

Cited by 252 publications

References 55 publications

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

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