scholarly journals Telomeres and Telomerase Activity in the Human Placenta

2020 ◽  
Author(s):  
Marie Jirkovská ◽  
Marie Korabečná ◽  
Soňa Laššáková
Keyword(s):  
Human Placenta ◽  
Telomerase Activity

Immortalized Human Placenta Derived Mesenchymal Cells by Transfection with Bmi-1 Lost the Abilitiy To Differencitate into Cell Types of Osteocytic, Condoricytic and Neural Lineages.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4259-4259
Author(s):  
Xiaohong Zhang ◽  
Yasushi Soda ◽  
Kenji Takahashi ◽  
Yuansong Bai ◽  
Koichi Igura ◽  
...  
Keyword(s):  
Human Placenta ◽  
Lentiviral Vector ◽  
Culture Media ◽  
Cell Types ◽  
Telomerase Activity ◽  
Mesenchymal Cells ◽  
Differentiation Potential ◽  
Chorionic Villi ◽  
Cd34 Cells ◽  
Infected Cells

Abstract Introduction: We previously reported that mesenchymal cells derived from chorionic villi of human placenta could differentiate into various cell types including osteocytic, condoricytic and neural lineages. However, these cells can slowly proliferate with limited life span. In the present study, we transduced human placenta-derived mesenchymal cells (PDMCs) with cDNA encoding Bmi-1 and telomerase reverse transferase (hTert), respectively or simultaneously by lentiviral vector, and tested transduced cells for their ability to differentiate into multi-lineages and to support expansion of CD34+ cells in cord blood as feeder cells in the presence of cytokine cocktails. Method: The lentivairal vector expressing either Bmi-1, hTert or hrGFP was prepared as previously. The human PDMCs were isolated from chorionic villi of human placenta using the explant culture, and were cultured in DMEM (low glucose) with 10% FBS. The established cells were infected with either of the three viruses or a combination of Bmi-1 and hTert virus at the multiplicity of infection that allowed almost 100% of infection efficiency based on hrGFP fluorescence by flow cytometry. Those infected cells and uninfected cells served as control were then continuously propagated. These cells were then transferred into the specific culture media to differentiate them to osteocyte, condorocyte and neural cells as reported previously. Results: The control and PDMC/hTert cells showed a broad and flat shape suggesting that these cells were senescence and ceased proliferation. Cells infected with Bmi-1 and Bmi-1/hTert escaped the crisis and continued proliferation. These cells have been maintained in culture for more than 1 year and continued to proliferate near to 100PD. We found that Bmi-1 over-expression could induce endogenous telomerase activity and elongate telomere length in PDMCs. The expression of p16 mRNA and protein were down-regulated in prolonged culture cells, but p14ARF was not. The differentiation potential of transduced cells was gradually lost as culture was prolonged as well as the ability to support the expansion of CB CD34+ cells. Gene expression analysis on Bmi-1- infected cells at different PD revealed that more than 100 genes were induced or repressed in several different functional categories.Extensive increase in expression of the IGFBP2 mRNA and higher concentration of IGFBP2 was observed. Conclusion: Bmi-1 induced Telomerase activity and immorlized human placenta derived mesenchymal cells. The ability of transduced cells to differentiate into various cell types and support expansion of CB CD34+ cells were lost with propagation suggesting that subtle transformation has occurred in the Bmi-1 transduced cells.

The transfer of pravastatin in the human placenta in women with Antiphospholipid Syndrome

2017 ◽  
Vol 77 (04) ◽  
pp. 379-395
Author(s):  
K Mayer-Pickel ◽  
M Gruber ◽  
B Hirschmugl ◽  
U Lang ◽  
M Cervar-Zivkovic ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Human Placenta

Inhibition of Platelet Aggregation by Human Placenta

1985 ◽  
Vol 54 (02) ◽  
pp. 431-437 ◽  
Author(s):  
M J Dembélé-Duchesne ◽  
A Laghchim Lahlou ◽  
H Thaler-Dao ◽  
A Crastes de Paulet
Keyword(s):  
Fatty Acid ◽  
Platelet Aggregation ◽  
Human Placenta ◽  
Cyclooxygenase Inhibitor ◽  
Synthetase Inhibitor ◽  
Inhibition Of Platelet Aggregation ◽  
Thromboxane Synthetase ◽  
Rabbit Platelets ◽  
High Doses ◽  
Induced Aggregation

SummaryHuman placental cytosol inhibits platelet aggregation induced by high doses of collagen. The aim of this study was to investigate whether this anti-aggregating activity was caused only by the presence of various activities already described in the placenta (an ADP-consuming enzyme, a fatty acid cyclooxygenase inhibitor, and a thromboxane synthetase inhibitor) or whether another factor was present.Heating the cytosol at 50° C for 6 min destroyed the inhibitor of collagen-induced aggregation. ADPase and the AA pathway inhibitors were not modified by this treatment. We therefore show the presence of an additional anti-aggregating factor: it is destroyed by heating at 50° C.We also tested for the presence of an inhibitor of AA release in the placental cytosol using three different methods (rabbit platelets in PRP, washed rabbit platelets, and NRK fibroblasts) but no inhibition could be evidenced.We conclude that this new anti-aggregating factor, which is probably a protein, acts neither through AA release inhibition nor AA cascade inhibition.

METABOLISM OF 17α-HYDROXYPROGESTERONE-4-14C-17α-CAPROATE BY HOMOGENATES OF RAT LIVER AND HUMAN PLACENTA

1961 ◽  
Vol 36 (4) ◽  
pp. 511-519 ◽  
Author(s):  
Margaret Wiener ◽  
Charles I. Lupa ◽  
E. Jürgen Plotz
Keyword(s):  
Rat Liver ◽  
Human Placenta ◽  
Steric Hindrance ◽  
Placental Tissue ◽  
Caproic Acid ◽  
Major Product ◽  
Side Chain ◽  
Anaerobic Conditions ◽  
Prolonged Action ◽  
Long Acting

ABSTRACT 17α-hydroxyprogesterone-4-14C-17α-caproate (HPC), a long-acting progestational agent, was incubated with homogenates of rat liver and human placenta. The rat liver was found to reduce Ring A of HPC under anaerobic conditions to form allopregnane-3β,17α-diol-20-one-17α-caproate and pregnane-3β,17α-diol-20-one-17α-caproate, the allopregnane isomer being the major product. The caproic acid ester was neither removed nor altered during the incubation. Placental tissue did not attack HPC under conditions where the 20-ketone of progesterone was reduced. It is postulated that this absence of attack on the side chain is due to steric hindrance from the caproate ester, and that this may account for the prolonged action of HPC.

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