Abstract
ObjectiveTelomeres stabilize and protect chromosomes from fusion and degradation. They are shortened by cellular senescence and stress. Telomere shortening was reported in leukocytes of diabetic patients and seems to be linked to diabetic complications. hTERT, the catalytic component of the enzyme telomerase and telomere capture are mechanisms responsible for telomere length. Dysfunctional telomeres tend to fuse and form aggregates. Senescence is associated with changes in the nuclear chromatin known as senescence-associated heterochromatin foci (SAHFs). Our aim was to assess telomere homeostasis in placentas from pregnancies complicated with diabetes.Study DesignPlacental biopsies from third trimester pregnancies complicated with diabetes (n=12) were compared with a control group of placentas from gestational age matched uncomplicated pregnancies (n=12). Telomeric parameters were evaluated: Telomere length, aggregates, SAHFs formation and telomere capture using manual and computerized Quantitative fluorescence-in-situ hybridization (Q-FISH). The amount of hTERT was evaluated using immunohistochemistry.ResultsDiabetic placentas expressed significantly shorter telomeres with increased aggregates and SAHFs formation and also increased expression of hTERT and telomere capture. (table).Tabled 1% Trophoblasts with the following parameters:ControlDiabetesP valueClear short telomeres4.92 ± 6.4224.42 ± 22.60.013Clear long telomeres90.92 ± 8.1370.17 ± 27.010.006Aggregates0.62 ± 0.872.75 ± 1.14<0.0001Nuclei with SAHFs8.77 ± 5.3119 ± 7.930.001Increased hTERT expression25.36 ± 5.2637 ± 9.690.001Evidence of telomere capture7.82 ± 2.9515.1 ± 8.450.014 Open table in a new tab ConclusionTelomeres are shorter in placentas from pregnancies complicated with diabetes, which might influence intrauterine programming of those fetuses. ObjectiveTelomeres stabilize and protect chromosomes from fusion and degradation. They are shortened by cellular senescence and stress. Telomere shortening was reported in leukocytes of diabetic patients and seems to be linked to diabetic complications. hTERT, the catalytic component of the enzyme telomerase and telomere capture are mechanisms responsible for telomere length. Dysfunctional telomeres tend to fuse and form aggregates. Senescence is associated with changes in the nuclear chromatin known as senescence-associated heterochromatin foci (SAHFs). Our aim was to assess telomere homeostasis in placentas from pregnancies complicated with diabetes. Telomeres stabilize and protect chromosomes from fusion and degradation. They are shortened by cellular senescence and stress. Telomere shortening was reported in leukocytes of diabetic patients and seems to be linked to diabetic complications. hTERT, the catalytic component of the enzyme telomerase and telomere capture are mechanisms responsible for telomere length. Dysfunctional telomeres tend to fuse and form aggregates. Senescence is associated with changes in the nuclear chromatin known as senescence-associated heterochromatin foci (SAHFs). Our aim was to assess telomere homeostasis in placentas from pregnancies complicated with diabetes. Study DesignPlacental biopsies from third trimester pregnancies complicated with diabetes (n=12) were compared with a control group of placentas from gestational age matched uncomplicated pregnancies (n=12). Telomeric parameters were evaluated: Telomere length, aggregates, SAHFs formation and telomere capture using manual and computerized Quantitative fluorescence-in-situ hybridization (Q-FISH). The amount of hTERT was evaluated using immunohistochemistry. Placental biopsies from third trimester pregnancies complicated with diabetes (n=12) were compared with a control group of placentas from gestational age matched uncomplicated pregnancies (n=12). Telomeric parameters were evaluated: Telomere length, aggregates, SAHFs formation and telomere capture using manual and computerized Quantitative fluorescence-in-situ hybridization (Q-FISH). The amount of hTERT was evaluated using immunohistochemistry. ResultsDiabetic placentas expressed significantly shorter telomeres with increased aggregates and SAHFs formation and also increased expression of hTERT and telomere capture. (table).Tabled 1% Trophoblasts with the following parameters:ControlDiabetesP valueClear short telomeres4.92 ± 6.4224.42 ± 22.60.013Clear long telomeres90.92 ± 8.1370.17 ± 27.010.006Aggregates0.62 ± 0.872.75 ± 1.14<0.0001Nuclei with SAHFs8.77 ± 5.3119 ± 7.930.001Increased hTERT expression25.36 ± 5.2637 ± 9.690.001Evidence of telomere capture7.82 ± 2.9515.1 ± 8.450.014 Open table in a new tab Diabetic placentas expressed significantly shorter telomeres with increased aggregates and SAHFs formation and also increased expression of hTERT and telomere capture. (table). ConclusionTelomeres are shorter in placentas from pregnancies complicated with diabetes, which might influence intrauterine programming of those fetuses. Telomeres are shorter in placentas from pregnancies complicated with diabetes, which might influence intrauterine programming of those fetuses.
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