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Abstract
BackgroundO‐linked β‐N‐acetylglucosamine (O‐GlcNAc) is a post‐translational modification that modulates several proteins related to the vascular tone control. Dysregulation of O‐GlcNAcylation occurs in a wide range of diseases, favoring endothelial dysfunction. During pregnancy, vascular dysfunction observed in the uterine vasculature results in inadequate nutritional support between the maternal‐fetal interface. It remains to be elucidated whether augmented O‐GlcNAc levels impact uterine artery (UA) function from virgin or pregnant rats.HypothesisIncreased O‐GlcNAc impairs the endothelial function of the uterine artery.MethodsPregnant or virgin Wistar rats (14‐week old) were treated either with glucosamine (300 mg/Kg) or vehicle, for 21 days, i.p. The UAs were rapidly removed, cleaned from fat tissue and mounted for isometric force development record. Concentration response‐curves to acetylcholine (1 nM to 100 μM) were performed in UA contracted with phenylephrine (10 μM), in the presence or absence of L‐NAME (100 μM, 30 minutes). Protein expression was evaluated by western blot.ResultsGlucosamine treatment increased O‐GlcNAc expression in UAs from virgin rats (p= 0.04). Decreased endothelium‐dependent relaxation was observed in UAs from treated virgin rats compared to vehicle [Emax 56.16 ± 4.18 vs. 76.38 ± 3.92%, respectively], which was abolished by incubation with L‐NAME. Endothelial nitric oxide synthase (eNOS) activity was decreased (p=0.04) by glucosamine‐treatment in virgin rats. On the other hand, in pregnancy, treatment with glucosamine decreased O‐GlcNAc expression (p=0.03) in UAs compared to vehicle. Increased sensitivity to acetylcholine [pD2 6.43 ± 0.13 vs. 6.90 ± 0.11] was observed in the UAs of glucosamine‐treated pregnant rats compared to vehicle pregnant rats with no differences in the maximal response. eNOS activity was unchanged between these groups.ConclusionsGlucosamine‐treatment impairs UA endothelial function in virgin, but not in pregnant rats.Support or Funding InformationCAPESFAPEGNIH (HL‐134604)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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