Ultrastructural features of cellular maturation and aging in human trophoblast

Martin, B. J.; Spicer, Samuel S.

doi:10.1016/s0022-5320(73)90074-9

Cited by 84 publications

(31 citation statements)

References 24 publications

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“…59,60 Frozen liver tissue was homogenized in a 2 ml dounce homogenenzer in 1.5 mM KCl, 2.5 mM MgCl 2 , 5 mM Tris, pH 7.5, 1% Triton X-100 and 1% sodium deoxycholate. Samples were spun at 2500 g for 15 min at 4 °C and the supernatant was collected.…”

Section: Animalsmentioning

confidence: 99%

Chronic rapamycin treatment or lack ofS6K1does not reduce ribosome activity in vivo

et al. 2013

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reducing activity of the mtorC1/S6K1 pathway has been shown to extend lifespan in both vertebrate and invertebrate models. For instance, both pharmacological inhibition of mtorC1 with the drug rapamycin or S6K1 knockout extends lifespan in mice. Since studies with invertebrate models suggest that reducing translational activity can increase lifespan, we reasoned that the benefits of decreased mtorC1 or S6K1 activity might be due, at least in part, to a reduction of general translational activity. Here, we report that mice given a single dose of rapamycin have reduced translational activity, while mice receiving multiple injections of rapamycin over 4 weeks show no difference in translational activity compared with vehicle-injected controls. Furthermore, mice lacking S6K1 have no difference in global translational activity compared with wild-type littermates as measured by the percentage of ribosomes that are active in multiple tissues. translational activity is reduced in S6K1-knockout mice following single injection of rapamycin, demonstrating that rapamycin's effects on translation can occur independently of S6K1. taken together, these data suggest that benefits of chronic rapamycin treatment or lack of S6K1 are dissociable from potential benefits of reduced translational activity, instead pointing to a model whereby changes in translation of specific subsets of mrNas and/or translation-independent effects of reduced mtor signaling underlie the longevity benefits.

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Section: Animalsmentioning

confidence: 99%

Chronic rapamycin treatment or lack ofS6K1does not reduce ribosome activity in vivo

et al. 2013

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“…Rather, the final consequence of apoptosis is nuclear aggregation and extrusion of groups of apoptotic nuclei together with some surrounding cytoplasm, forming the so-called syncytial sprouts ( Fig. 8; Martin and Spicer 1973;Jones and Fox 1977;Cantle et al 1987). The latter are likely to be the syncytial correlate of apoptotic bodies (Fig.…”

Section: Evidence For the Apoptotic Cascade In The Syncytiotrophoblastmentioning

confidence: 99%

“…Most syncytial "sprouts" in the human placenta are not due to true villous sprouting (Cantle et al 1987;Castellucci et al 1990), rather they result from the accumulation of aged nuclei (Martin and Spicer 1973;Jones and Fox 1977;Cantle et al 1987; for review see Benirschke and Kaufmann 1995) prior to extrusion into the maternal circulation. Syncytial nuclei demonstrating advanced features of apoptosis were mostly confined to these structures (Figs.…”

Section: Syncytial Fusion Retards Syncytiotrophoblast Apoptosismentioning

confidence: 99%

Villous cytotrophoblast regulation of the syncytial apoptotic cascade in the human placenta

Huppertz¹,

Frank²,

et al. 1998

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Villous trophoblast in the human placenta consists of a population of proliferating stem cells which differentiate and individually fuse into the syncytiotrophoblast. We studied the apoptotic cascade in this complex epithelial layer by immunohistochemical localization of Fas, FasL, Bcl-2, Mcl-1, pro-caspase-3 and caspase-3, T-cell-restricted intracellular antigen-related protein (TIAR), poly(ADP-ribose) polymerase (PARP), lamin B, topoisomerase IIalpha, and transglutaminase II in cryostat and paraffin-fixed tissue sections from normal human first-trimester and term placental villi. The relationship between the apoptotic cascade and syncytial fusion was studied by coincubation of intact villi with FITC-coupled annexin-V, to detect the phosphatidylserine flip, and propidium iodide, to detect plasma membrane permeability. The final events of the apoptotic cascade were studied by the TUNEL reaction and ultrastructural appearance of the trophoblast. The phosphatidylserine flip was identified in some of the villous cytotrophoblastic cells, but the presence of both Bcl-2 and Mcl-1 proteins presumably prevented continuation of the apoptotic cascade. The syncytiotrophoblast demonstrated heterogeneous findings, suggesting variable progression along the apoptotic cascade. In some areas Bcl-2 and Mcl-1 predominated, with preservation of the nuclear proteins PARP, lamin B, and topoisomerase IIalpha; in other areas, especially in and around syncytial sprouts, Bcl-2 and Mcl-1 were absent, accompanied by loss of nuclear proteins, presence of phosphatidylserine flip, and TUNEL positivity. These data suggest that the apoptotic cascade is initiated in the villous cytotrophoblast, which in turn promotes syncytial fusion. Donation of anti-apoptotic proteins into the syncytium, such as Bcl-2 and Mcl-1, focally inhibits further progression along this cascade. Completion of the apoptotic cascade takes place in and around syncytial sprouts, providing further evidence that these are the sites of trophoblast shedding into the maternal circulation.

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“…Increased number of syncytiotrophoblast nuclei was noted in the diabetic group (Martin & Spicer, 1973;Jones & Fox). Small focal areas of necrosis, variable degree of dilatation of rough endoplasmic reticulum and autophagic vacuoles was also observed in few placentas (Jones & Fox) In our study, we observed more number of syncytial knots, dilatation of rough endoplasmic reticulum and Glycogen deposits in the syncytium in majority of cases.…”

mentioning

confidence: 88%

Ultrastructural Changes in the Placental Membrane in Pregnancies Associated with Diabetes

Verma¹,

Mishra²,

Kaul³

2011

Int. J. Morphol.

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Cambios Ultraestructurales en la Membrana Placentaria en Embarazos Asociados con la DiabetesRanjana SUMMARY:Placenta is the most accurate record of the infant prenatal experience. If the placenta is examined minutely after delivery, it provides much insight into the prenatal health of the baby and the mother. The weight of placenta is higher in diabetic pregnancy in comparison to the normal pregnancy. To study the cellular changes that might contribute to more weight of placenta in diabetic pregnancies, light microscopic and electron microscopic analysis was performed. Twenty singleton pregnancies complicated with Gestational diabetes mellitus (12 controlled on diet, 8 controlled on insulin) were selected and compared to control group. Tissue sections were processed and analyzed. The placenta of diabetic pregnancies showed no abnormality on gross observation but light microscopic examination revealed, lesions like syncytial knots, fibrinoid necrosis, villous edema, villous fibrosis and capillary proliferation. Transmission electron microscopic examination (TEM) showed changes in almost all the layers of the placental membrane i.e. synctiotrophoblast, cytotrophoblast, trophoblastic basement membrane and fetal capillaries. These changes were observed in the placenta of both groups of patients whether blood sugar level was controlled by diet or insulin, but to different degree. It indicates that control of hyperglycemia only partially prevents the development of placental abnormalities which must be due to some other constituent factor of diabetic state. KEY WORDS: Gestational diabetes mellitus; Transmission electron Microscopy; Placental membrane. INTRODUCTIONDiabetes is now a major health concern in our society. According to the centers for disease control and prevention, from 1980 to 2005, the crude incidence of diagnosed diabetes has increased from 3.3 per 1000 to 7.4 per 1000 i.e by 124%. Studies suggest that the prevalence of diabetes mellitus (DM) among women of childbearing age is increasing due to more sedentary lifestyles, changes in diet, and the virtual epidemic of childhood and adolescent obesity that is presently evolving in India. Gestational diabetes mellitus (GDM) is defined as glucose intolerance of variable degree with onset or first recognition during pregnancy. Abnormal maternal glucose tolerance occurs in 3-10% of pregnancies in Indian population (Dutta, 2004).Maternal diabetes mellitus exposes the fetus to the risk of macrosomia, congenital malformations, intrauterine growth retardation and difficult labour (Fletcher, 1981). The neonatal metabolic problems are hypoglycemia and hypocalcaemia. All these conditions may be related to reduced placental perfusion and decreased arterial oxygen saturation attributing to placental abnormalities. Therefore, the placenta of diabetic women has gained much interest showing several pathological changes.In term pregnancy, the placental membrane is extremely thin, approximately 0.002mm in thickness, separating fetal blood from maternal blood. The five layers...

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Ultrastructural features of cellular maturation and aging in human trophoblast

Cited by 84 publications

References 24 publications

Chronic rapamycin treatment or lack ofS6K1does not reduce ribosome activity in vivo

Chronic rapamycin treatment or lack ofS6K1does not reduce ribosome activity in vivo

Villous cytotrophoblast regulation of the syncytial apoptotic cascade in the human placenta

Ultrastructural Changes in the Placental Membrane in Pregnancies Associated with Diabetes

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