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Journals / Medical Records / 2026 / Cilt: 5 Sayı: 2

Oxidative Stress Elevates eNOS Expression and VSMCs Proliferation of the Umbilical Vein of GDM Mothers

Wulamujiang Aini(KOCAELI UNIVERSITY, CLINICAL AND EXPERIMENTAL STUDIES APPLICATION AND RESEARCH CENTER)0000-0001-5945-0725
Candan Yılmaz Özdoğan(KOCAELI UNIVERSITY, CLINICAL AND EXPERIMENTAL STUDIES APPLICATION AND RESEARCH CENTER)0000-0001-5885-4189
Gamze Kara Mağden(KOCAELI UNIVERSITY, CLINICAL AND EXPERIMENTAL STUDIES APPLICATION AND RESEARCH CENTER)0000-0002-8063-3726
Emek Doğer(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF SURGICAL MEDICAL SCIENCES, DEPARTMENT OF OBSTETRICS AND GYNAECOLOGY, GYNECOLOGICAL ONCOLOGY)0000-0002-8941-5469
Vildan Küçükoğlu(KOCAELI UNIVERSITY, CLINICAL AND EXPERIMENTAL STUDIES APPLICATION AND RESEARCH CENTER)0000-0002-5400-9743
Bahar Muezzinoglu(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF SURGICAL MEDICAL SCIENCES, DEPARTMENT OF PATHOLOGY)0000-0001-6080-0673
Büşra Özbek(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF SURGICAL MEDICAL SCIENCES, DEPARTMENT OF PATHOLOGY)0000-0002-4221-0845
Zeynep Cantürk(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, ENDOCRINOLOGY AND METABOLIC DISEASES)0000-0001-7114-2565
Berrin Çetinaslan(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, ENDOCRINOLOGY AND METABOLIC DISEASES)0000-0002-8041-8161
İlhan Tarkun(KOCAELI UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, DEPARTMENT OF INTERNAL MEDICINE, ENDOCRINOLOGY AND METABOLIC DISEASES)0000-0002-3529-7495
Halime Kenar(KOCAELI UNIVERSITY, CLINICAL AND EXPERIMENTAL STUDIES APPLICATION AND RESEARCH CENTER)0000-0003-0433-5513
Pages
269–76
Publication Date
2023-05-15
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Increased oxidative stress, which elevates eNOS expression and VSMC proliferation in the umbilical vessels of mothers with GDM, may be a sign that mothers have a high potential for developing diabetes or cardiovascular disease in the future.

📌 3 Key Takeaways

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Objective & Hypothesis:Aim: Gestational diabetes mellitus (GDM) is associated with an increased risk of fetal and maternal complications, such astype 2 DM (diabetes mellitus) and cardiovascular disease (CVD).
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Key Findings & Data:Material and Methods: Subjects were divided into two groups: the normoglycemic control (NGC) group (n = 10) and the GDM group (n = 12).
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Conclusion & Impact:Conclusion: Increased oxidative stress, which elevates eNOS expression and VSMC proliferation in the umbilical vessels of mothers with GDM, may be a sign that mothers have a high potential for developing diabetes or cardiovascular disease in the future.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:GDM · oxidative stress · VSMCs

Abstract

Aim: Gestational diabetes mellitus (GDM) is associated with an increased risk of fetal and maternal complications, such astype 2 DM (diabetes mellitus) and cardiovascular disease (CVD). This study aimed to predict the potential for future vascular complications in mothers with GDM by evaluating oxidative stress, endothelial NO synthase (eNOS) expression, and vascular smooth muscle cell (VSMC) proliferation in the umbilical vessels of mothers with GDM. Material and Methods: Subjects were divided into two groups: the normoglycemic control (NGC) group (n = 10) and the GDM group (n = 12). Expression of eNOS and production of reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs) were determined. The mitochondrial mass of HUVECs was evaluated by spectrofluorometry. VSMC proliferation was ascertained in vitro with an EdU cell proliferation assay. Advanced glycation end products (AGEs) accumulation was measured by ELISA and assessed by immunohistochemical staining Results: VSMC proliferation, eNOS expression, and ROS production in HUVECs were significantly increased, and greater immunohistochemical staining to AGEs was observed in endothelium in GDM. Conclusion: Increased oxidative stress, which elevates eNOS expression and VSMC proliferation in the umbilical vessels of mothers with GDM, may be a sign that mothers have a high potential for developing diabetes or cardiovascular disease in the future.

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Cite This Article

Aini, W., Özdoğan, C. Y., Mağden, G. K., Doğer, E., Küçükoğlu, V., Muezzinoglu, B., Özbek, B., Cantürk, Z., Çetinaslan, B., Tarkun, İ., Kenar, H. (2023). Oxidative Stress Elevates eNOS Expression and VSMCs Proliferation of the Umbilical Vein of GDM Mothers. Medical Records, Cilt: 5 Sayı: 2, 269–76. https://doi.org/10.37990/medr.1195487

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References (20)

  1. REFERENCES 1. World Health Organisation. Global Report on Diabetes. WHO Press; Geneva, Switzerland: 2016.
  2. Anna V, Van Der Ploeg HP, Cheung NW, et al. Sociodemographic correlates of the increasing trend in the prevalence of gestational diabetes mellitus in a large population of women between 1995 and 2005. Diabetes care. 2008; 31: 2288-93.
  3. Negre-Salvayre A, Salvayre R, Auge N, et al. Hyperglycemia and glycation in diabetic complications. Antioxid Redox Signal. 2009; 11: 3071-109.
  4. Yamagishi Si, Nakamura K, Matsui T, et al. Agents that block advanced glycation end product (AGE)-RAGE (receptor for AGEs)-oxidative stress system: a novel therapeutic strategy for diabetic vascular complications. Expert Opin Investig Drugs. 2008; 17: 983-96.
  5. Cooper ME, Bonnet F, Oldfield M, Jandeleit-Dahm K. Mechanisms of diabetic vasculopathy: an overview. Am J Hypertens. 2001; 14: 475-86.
  6. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 2001; 414: 813-20. 7. Maiese K. New insights for oxidative stress and diabetes mellitus. Oxid Med Cell longev 2015. doi: 10.1155/2015/875961.
  7. Förstermann U, Xia N, Li, H. Roles of vascular oxidative stress and nitric oxide in the pathogenesis of atherosclerosis. Circ Res. 2017; 120: 713-35.
  8. Krizbai IA, Bauer H, Bresgen N, et al. Effect of oxidative stress on the junctional proteins of cultured cerebral endothelial cells. Cell Mol Neurobiol. 2005; 25:129-39.
  9. Babawale M, Lovat S, Mayhew T, et al. Effects of gestational diabetes on junctional adhesion molecules in human term placental vasculature. Diabetologia. 2000; 43: 1185-96. 11. Sobrevia L. Placenta. Trophoblast Research. Preface. Placenta 2011; 32: S78-80. 12. Shen GX. Oxidative stress and diabetic cardiovascular disorders: roles of mitochondria and NADPH oxidase. Can J Physiol Pharmacol. 2010; 88: 241-8.
  10. Shi N, Chen SY. Mechanisms simultaneously regulate smooth muscle proliferation and differentiation. J Biomed Res. 2014; 28: 40. doi: 10.7555/JBR.28.20130130.
  11. Han RN, Stewart DJ. Defective lung vascular development in endothelial nitric oxide synthase-deficient mice. Trends Cardiovasc Med. 2006; 16: 29-34.
  12. Cai S, Khoo J, Channon KM. Augmented BH4 by gene transfer restores nitric oxide synthase function in hyperglycemic human endothelial cells. Cardiovasc Res. 2005; 65: 823-31.
  13. Holt R, Coleman M, McCance D. The implications of the new International Association of Diabetes and Pregnancy Study Groups (IADPSG) diagnostic criteria for gestational diabetes. Diabet Med: A Journal of the British Diabetic Association. 2011; 28: 382-5.
  14. Subiabre M, Silva L, Toledo F, et al. Insulin therapy and its consequences for the mother, fetus, and newborn in gestational diabetes mellitus. Biochim Biophys Acta 2018; 1864: 2949-56. 18. Sultan SA, Liu W, Peng Y, et al. The role of maternal gestational diabetes in inducing fetal endothelial dysfunction. J Cell Physiol. 2015; 230: 2695-705.
  15. Taniyama Y, Griendling KK. Reactive oxygen species in the vasculature: molecular and cellular mechanisms. Hypertension. 2003; 42: 1075-81.
  16. Velarde V, De La Cerda PM, Duarte C, et al. Role of reactive oxygen species in the bradykinin-induced proliferation of vascular smooth muscle cells. Biol Res. 2004; 37: 419-30. 21. Faries PL, Rohan DI, Takahara H, et al. Human vascular smooth muscle cells of diabetic origin exhibit increased proliferation, adhesion, and migration. J Vasc Surg 2001; 33: 601-7.
  17. Rivard A, Andrés V. Vascular smooth muscle cell proliferation in the pathogenesis of atherosclerotic cardiovascular diseases. Histol Histopathol. 2000; 15:557-71.
  18. Förstermann U, Li H. The therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling. Br J Pharmacol. 2011; 164: 213-23.
  19. Adela R, Nethi SK, Bagul PK, et al. Hyperglycaemia enhances nitric oxide production in diabetes: a study from South Indian patients. PloS one. 2015; 10: e0125270. doi: 10.1371/journal.pone.0125270.
  20. Kostopoulou E, Kalaitzopoulou E, Papadea P, et al. Oxidized lipid-associated protein damage in children and adolescents with type 1 diabetes mellitus: New diagnostic/prognostic clinical markers. Pediatr Diabetes. 2021; 22:1135-42.