SavedAdd your journal

Journals / SDÜ Tıp Fakültesi Dergisi / 2026 / Cilt: 28 Sayı: 1

THE EFFECTS OF IMMOBILIZATION STRESS ON PLACENTA AND FETUS IN PREGNANT MICE

FARE GEBELİK DÖNEMİNDE HAREKETSİZLİK STRESİNİN PLASENTA VE YAVRUYA ETKİLERİ

Nihan Semerci(Department of Obstetrics and Gynecology, University of South Florida, Morsani College of Medicine)
Gökçen Bilici(Department of Histology and Embryology, Dokuz Eylul University, School of Medicine)0000-0003-0027-9286
Filiz Yılmaz(Department of Histology and Embryology, Dokuz Eylul University, School of Medicine)0000-0003-0505-3905
Zahide Çavdar(DOKUZ EYLUL UNIVERSITY)0000-0002-5457-198X
Uygar Sacık(ANKARA YILDIRIM BEYAZIT UNIVERSITY)0000-0002-3154-8779
Ümit Kayışlı(Department of Obstetrics and Gynecology, University of South Florida, Morsani College of Medicine, Tampa, Florida, USA)
Guven Erbil(Department of Histology and Embryology, Dokuz Eylul University, School of Medicine)0000-0002-8448-0691
Pages
31–39
Publication Date
2021-03-11
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

CONCLUSION: Gestational stress causes placental dysfunctions by triggering apoptosis, reducing the labyrinth zone as well as increasing collagen levels, which may impair fetal development that may contribute to pathogenesis of intrauterine growth restriction.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:ABSTRACT AIM: Stress can affect negatively mother and fetuses during pregnancy.
📊
Key Findings & Data:MATERİALS AND METHODS: Balb/c virgin female mice (20-30 g) were mated with male mice in a 2 to 1 female to male ratio.
💡
Conclusion & Impact:CONCLUSION: Gestational stress causes placental dysfunctions by triggering apoptosis, reducing the labyrinth zone as well as increasing collagen levels, which may impair fetal development that may contribute to pathogenesis of intrauterine growth restriction.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:Fetus · hareketsizlik stresi · plasenta

Abstract

ABSTRACT AIM: Stress can affect negatively mother and fetuses during pregnancy. We aimed to investigate the effects of chronic immobilization stress on placental maturation and fetal development. MATERİALS AND METHODS: Balb/c virgin female mice (20-30 g) were mated with male mice in a 2 to 1 female to male ratio. Pregnant mice in control group (n=6) were left undisturbed, whereas pregnant mice in the stress group (n=6) were exposed to 45 min chronic immobilization stress for three times/day starting from gestational day 6 till 18. Fetuses and placentas were removed from dams on the gestational day 18 under anesthesia. RESULTS: The prenatal stress significantly increased apoptosis in several placental cells including trophoblastic giant cells, glycogen cells and labyrinth trophoblastic cells and resulted in intrauterine growth restriction. The stress caused a decreased superoxide dismutase and glutathione levels. Alizarin Red S staining shows the ossification center of the fetuses to see developmental abnormality. CONCLUSION: Gestational stress causes placental dysfunctions by triggering apoptosis, reducing the labyrinth zone as well as increasing collagen levels, which may impair fetal development that may contribute to pathogenesis of intrauterine growth restriction.

Özet

ÖZ AMAÇ: Stres gebelik sürecinde anne ve fetüs sağlığını olumsuz etkilemektedir. Çalışmamızda kronik hareketsizlik stresinin plasenta ve fetüs gelişimi üzerine etkilerini araştırmayı hedefledik. GEREÇ VE YÖNTEMLER: Balb/c suşu dişi fareler (20-30gr), 2dişi-1erkek olacak şekilde katıma alındı. Kontrol grubundaki (n=6) gebe farelere herhangi bir uygulama yapılmazken, stres grubundaki (n=6) gebe farelere gebeliğin 6.gününden 18.gününe kadar günde 3 defa 45dakikalık kronik hareketsizlik stresine maruz bırakıldı. Gebeliğinin 18. Gününde plasenta ve fetüsler anestezi altında sezaryen ile alındı. BULGULAR: Prenatal stres, trofoblastik dev hücreler, glikojen içeren hücreler ve labirent trofoblastik hücreler dahil olmak üzere birçok plasental hücrede apoptozu önemli ölçüde arttırdı ve intrauterin büyüme geriliğine sebep oldu. Stres süperoksit dismutaz ve glutatyon seviyelerini azalttı. Fetüsün gelişimini değerlendirmek için, Alizarin Red S boyaması ile fetüsün kemikleşme merkezleri değerlendirildi. SONUÇ: Gebelik sürecindeki stres, apoptozu tetikleyerek, labirent bölgesi küçüldü ve plasenta yetmezliğine sebep oldu, ayrıca kollajen seviyelerini arttırarak fetüs gelişimini olumsuz yönde etkileyerek intrauterin büyüme geriliği patogenezinde katkısı olduğunu gözlemledik.

🔖

Cite This Article

Semerci, N., Bilici, G., Yılmaz, F., Çavdar, Z., Sacık, U., Kayışlı, Ü., Erbil, G. (2021). THE EFFECTS OF IMMOBILIZATION STRESS ON PLACENTA AND FETUS IN PREGNANT MICE. SDÜ Tıp Fakültesi Dergisi, Cilt: 28 Sayı: 1, 31–39. https://doi.org/10.17343/sdutfd.651091

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (33)

  1. Referans1) Watson ED, Cross JC. Development of structures and transport functions in the mouse placenta, Physiology (Bethesda). 2005 Jun;20:180-93.
  2. Referans2) Jefferey MR, Yasuhiro Y, Monika AW, Abby CC. Placental inflammation and oxidative stress in the mouse model of assisted reproduction, Placenta. 2011 Nov; 32(11): 852–858. Published online 2011 Sep 1. doi: 10.1016/j.placenta.2011.08.003
  3. Referans3) Herman, J.P., Mcklveen J.M., Ghosal S. et al. Regulation of the hypothalamic-pituitary-adrenocortical stress response, Compr. Physiol. 6 (2016) 603–621. doi:10.1002/cphy.c150015.
  4. Referans4) Harris R.B.S., Chronic and acute effects of stress on energy balance: are there appropriate animal models?, Am. J. Physiol. - Regul. Integr. Comp. Physiol. 308 (2015) R250–R265. doi:10.1152/ajpregu.00361.2014
  5. Referans5) Perkinsa G., Bossy-Wetzelb E., Ellisman M.H., New Insights into Mitochondrial Structure during Cell Death, Exp. Neurol. 218 (2010) 183–192. doi:10.1016/j.expneurol.2009.05.021.
  6. Referans6) Straszewski-Chavez S.L., Abrahams V.M., Mor G., The role of apoptosis in the regulation of trophoblast survival and differentiation during pregnancy, Endocr. Rev. 26 (2005) 877–897. doi:10.1210/er.2005-0003.
  7. Referans7) Uckan D., Steele A., Cherry et al. Trophoblasts express Fas ligand: a proposed mechanism for immune privilege in placenta and maternal invasion., Mol. Hum. Reprod. 3 (1997) 655–662. doi:10.1093/molehr/3.8.655.
  8. Referans8) Huppertz B., Frank H.G., Kingdom J.C.P., Reister F., Kaufmann P., Villous cytotrophoblast regulation of the syncytial apoptotic cascade in the human placenta, Histochem. Cell Biol. 110 (1998) 495–508. doi:10.1007/s004180050311.
  9. Referans9) Demir R., İnsan plasentasında ışık mikroskobu, tarayıcı elektron mikroskobu bulguları ve ikizlerde perfüzyon incelemeleri, 1978.
  10. Referans10) Burtis C.A., Ashwood E.R., Tietz textbook of clinical chemistry, W.B. Saunders Company, Pennsylvania, 1994
  11. Referans11) Benirschke K., The placenta in the litigation process, Am. J. Obstet. Gynecol. 162 (1990) 1445–1450. doi:10.1016/0002-9378(90)90904-L.
  12. Referans12) Benirschke K., Kaufmann P., Baergen R.N., Abortion, placentas of trisomies, and immunologic considerations of recurrent reproductive failure, in: Pathol. Hum. Placenta, 2006: pp. 762–796.
  13. Referans13) Kaufmann P., Demonstration os cytoplasmic polyps from the human trophoblast by scanning electron microscopy, Arch. Gynakol. 211 (1970) 523.
  14. Referans14) Schulze B., Schlesinger C., Miller K., Chromosomal mosaicism confined to chorionic tissue, Prenat. Diagn. 7 (1987) 451–453. doi:10.1016/j.ajpath.2011.02.031.
  15. Referans15) Demir R., Demir A.Y, Yinanc M., Structural changes in placental barrier of smoking mother a quantitative and ulstrastructural study, Pathol. - Res. Pract. 190 (1994) 656–667. doi:10.1016/S0344-0338(11)80744-2.
  16. Referans16) Rassoulzadegan M., Rosen B.S., Gillot I., Cuzin F., Phagocytosis reveals a reversible differentiated state early in the development of the mouse embryo., EMBO J. 19 (2000) 3295–3303. doi:10.1093/emboj/19.13.3295.
  17. Referans17) El-Hashash A.H.K., Warburton D., Kimber S.J., Genes and signals regulating murine trophoblast cell development, Mech Dev. 127 (2010) 1–20. doi:10.1007/s11103-011-9767-z.Plastid.
  18. Referans18) Chakraborty D., Rumi M.A.K., Soares M.J., NK cells, hypoxia and trophoblast cell differentiation, Cell Cycle. 11 (2012) 2427–2430. doi:10.4161/cc.20542.
  19. Referans19) Nadeau V., Bissonauth V., Charron J., Le rôle des kinases Mek1 et Mek2 dans la formation de la barrière hématoplacentaire chez la souris, (2012).
  20. Referans20) Girardin F., Membrane transporter proteins: A challenge for CNS drug development, Dialogues Clin. Neurosci. 8 (2006) 311–321. doi:10.1016/0266-7681(94)90280-1.
  21. Referans21) Wataganara T., Bianchi D.W., Fetal cell-free nucleic acids in the maternal circulation: New clinical applications, Ann. N. Y. Acad. Sci. 1022 (2004) 90–99. doi:10.1196/annals.1318.015.
  22. Referans22) Gavrieli Y., Sherman Y., Ben-Sasson S.A., Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation, J. Cell Biol. 119 (1992) 493–501. doi:10.1083/jcb.119.3.493.
  23. Referans23) D’mello A.P., Liu Y., Effects of maternal immobilization stress on birth weight and glucose homeostasis in the offspring, Psychoneuroendocrinology. 31 (2006) 395–406. doi:10.1016/j.psyneuen.2005.10.003.
  24. Referans24) Molehin D., Dekker Nitert M., Richard K., Prenatal Exposures to Multiple Thyroid Hormone Disruptors: Effects on Glucose and Lipid Metabolism, J. Thyroid Res. 2016 (2016). doi:10.1155/2016/8765049.
  25. Referans25) Mairesse J., Lesage J., Breton C., et al. Maternal stress alters endocrine function of the feto-placental unit in rats, AJP Endocrinol. Metab. 292 (2007) E1526–E1533. doi:10.1152/ajpendo.00574.2006.
  26. Referans26) Morrison J.L., Sheep models of intrauterine growth restriction: Fetal adaptations and consequences, Clin. Exp. Pharmacol. Physiol. 35 (2008) 730–743. doi:10.1111/j.1440-1681.2008.04975.x.
  27. Referans27) Jang E.A., Longo L.D., Goyal R., Antenatal maternal hypoxia: criterion for fetal growth restriction in rodents., Front. Physiol. 6 (2015) 176. doi:10.3389/fphys.2015.00176.
  28. Referans28) Dimasuay K.G., Boeuf P., Powell T.L., Jansson T., Placental responses to changes in the maternal environment determine fetal growth, Front. Physiol. 7 (2016) 1–9. doi:10.3389/fphys.2016.00012.
  29. Referans29) Gundogan F., Elwood G., Mark P., Feijoo A., Longato L., Ethanol-induced oxidative stress and mitochondrial dysfunction in rat placenta: Relevance to Pregnancy Loss, Alcohol. Clin. Exp. Res. 34 (2010) 415–423. doi:10.1111/j.1530-0277.2009.01106.x.Ethanol-Induced.
  30. Referans30) Neale D.M., Mor G., The role of Fas mediated apoptosis in preeclampsia, J. Perinat. Med. 33 (2005) 471–477. doi:10.1515/JPM.2005.085.
  31. Referans31) Yasemin Aksoy, The Role Of Glutathıone In Antıoxıdant Mechanısm, Turkiye Klinikleri J Med Sci. 2002;22(4):442-8.
  32. Referans32) Murat Baflar, Mehmet Türker, Tülay İrez, Oktay Arda, Süperovulasyon Protokolünde Kullanılan GnRH Agonistinin Oosit Olgunluğu ve Çapına Etkileri, Cerrahpaşa Tıp Dergisi 2008; 39(2): 41-48 ISSN: 1300-5227.
  33. Referans33) Erica D. Watson, James C. Cross, Development of Structures and Transport Functions in the Mouse Placenta, Physiology (Bethesda). 2005 Jun;20:180-93.