Objective: 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.

Methods: 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.

Results: Diabetic placentas expressed significantly shorter telomeres with increased aggregates and SAHFs formation and also increased expression of hTERT and telomere capture. (table).

Conclusions: Telomeres are shorter in placentas from pregnancies complicated with diabetes, which might influence intrauterine programming of those fetuses.

Authors:

Tal Biron-Shental^a,b, Sefi Zargarian^c,d, Hanna Nabwani^a,b, Dvora Kidron^b,e, Moshe D. Fejgin^a,b,c, Aliza Amiel^c,d

^aDepartment of OBGYN department, Meir Medical Center

^bSackler School of Medicine, Tel Aviv University, Tel Aviv

 ^cGenetic Institute, Meir Hospital, Kfar-Saba

 ^dFaculty of Life Science, Bar-Ilan University, Ramat Gan

^eDeaprtment fo Pathology, Meir Hospital, Kfar-Saba.