715: Telomeres are shorter in placentas from pregnancies with uncontrolled diabetes

Abstract

ObjectiveIntrauterine environment, which is determined by different factors including diabetes in pregnancy, has an influence on lifetime morbidity. The placenta has a noteworthy impact on this process. Senescence is a state of cellular metabolic arrest, known to be correlated with age related diseases and is commonly accompanied by short telomeres. We studied telomere characteristics in placentas and in cord blood from term pregnancies complicated with uncontrolled diabetes mellitus.Study DesignPlacental biopsies and cord blood were collected from 16 pregnancies with poorly controlled diabetes and from 16 healthy controls. Senescence associated heterochromatin foci (SAHF) and senescence-associated β-galactosidase (SAβ-Gal) staining were evaluated. Apoptosis was evaluated using tunnel staining. Telomere length and aggregate formation were assessed in placentas and in cord blood using Q-FISH.ResultsIncreased SAHF (19.28%±7.93 Vs. 7.78%±5.31, P<0.001) and SAβ-Gal (7.1%±1.32 Vs. 0.8%±0.41, P<0.001) but not apoptosis were present in diabetic placentas compared to controls. Higher percentage of trophoblasts with short telomeres (24.42%±12.6 Vs. 4.92%±6.4, P=0.013) and noticeable more aggregate formation (2.75%±1.14 Vs. 0.62%±0.87, P<0.001) were observed in diabetic placentas when compared to healthy controls. These differences were not observed in cord blood samples.ConclusionPoorly controlled diabetes exposes increased senescence and shorter telomeres in placentas. Those findings may partially explain increased long term related morbidity. ObjectiveIntrauterine environment, which is determined by different factors including diabetes in pregnancy, has an influence on lifetime morbidity. The placenta has a noteworthy impact on this process. Senescence is a state of cellular metabolic arrest, known to be correlated with age related diseases and is commonly accompanied by short telomeres. We studied telomere characteristics in placentas and in cord blood from term pregnancies complicated with uncontrolled diabetes mellitus. Intrauterine environment, which is determined by different factors including diabetes in pregnancy, has an influence on lifetime morbidity. The placenta has a noteworthy impact on this process. Senescence is a state of cellular metabolic arrest, known to be correlated with age related diseases and is commonly accompanied by short telomeres. We studied telomere characteristics in placentas and in cord blood from term pregnancies complicated with uncontrolled diabetes mellitus. Study DesignPlacental biopsies and cord blood were collected from 16 pregnancies with poorly controlled diabetes and from 16 healthy controls. Senescence associated heterochromatin foci (SAHF) and senescence-associated β-galactosidase (SAβ-Gal) staining were evaluated. Apoptosis was evaluated using tunnel staining. Telomere length and aggregate formation were assessed in placentas and in cord blood using Q-FISH. Placental biopsies and cord blood were collected from 16 pregnancies with poorly controlled diabetes and from 16 healthy controls. Senescence associated heterochromatin foci (SAHF) and senescence-associated β-galactosidase (SAβ-Gal) staining were evaluated. Apoptosis was evaluated using tunnel staining. Telomere length and aggregate formation were assessed in placentas and in cord blood using Q-FISH. ResultsIncreased SAHF (19.28%±7.93 Vs. 7.78%±5.31, P<0.001) and SAβ-Gal (7.1%±1.32 Vs. 0.8%±0.41, P<0.001) but not apoptosis were present in diabetic placentas compared to controls. Higher percentage of trophoblasts with short telomeres (24.42%±12.6 Vs. 4.92%±6.4, P=0.013) and noticeable more aggregate formation (2.75%±1.14 Vs. 0.62%±0.87, P<0.001) were observed in diabetic placentas when compared to healthy controls. These differences were not observed in cord blood samples. Increased SAHF (19.28%±7.93 Vs. 7.78%±5.31, P<0.001) and SAβ-Gal (7.1%±1.32 Vs. 0.8%±0.41, P<0.001) but not apoptosis were present in diabetic placentas compared to controls. Higher percentage of trophoblasts with short telomeres (24.42%±12.6 Vs. 4.92%±6.4, P=0.013) and noticeable more aggregate formation (2.75%±1.14 Vs. 0.62%±0.87, P<0.001) were observed in diabetic placentas when compared to healthy controls. These differences were not observed in cord blood samples. ConclusionPoorly controlled diabetes exposes increased senescence and shorter telomeres in placentas. Those findings may partially explain increased long term related morbidity. Poorly controlled diabetes exposes increased senescence and shorter telomeres in placentas. Those findings may partially explain increased long term related morbidity.