DSpace Repository

FARE GEBELİK DÖNEMİNDE HAREKETSİZLİK STRESİNİN PLASENTA VE YAVRUYA ETKİLERİ

Show simple item record

dc.creator SEMERCİ, Nihan; Department of Obstetrics and Gynecology, University of South Florida, Morsani College of Medicine
dc.creator BİLİCİ, Gökçen; Department of Histology and Embryology, Dokuz Eylul University, School of Medicine
dc.creator YILMAZ, Filiz; Department of Histology and Embryology, Dokuz Eylul University, School of Medicine
dc.creator ÇAVDAR, Zahide; DOKUZ EYLUL UNIVERSITY
dc.creator SACIK, Uygar; ANKARA YILDIRIM BEYAZIT UNIVERSITY
dc.creator KAYIŞLI, Ümit; Department of Obstetrics and Gynecology, University of South Florida, Morsani College of Medicine, Tampa, Florida, USA
dc.creator ERBİL, Guven; Department of Histology and Embryology, Dokuz Eylul University, School of Medicine
dc.date 2021-03-11T00:00:00Z
dc.date.accessioned 2021-12-03T11:47:00Z
dc.date.available 2021-12-03T11:47:00Z
dc.identifier https://dergipark.org.tr/tr/pub/sdutfd/issue/60659/651091
dc.identifier 10.17343/sdutfd.651091
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/94206
dc.description ÖZ AMAÇ: Stres gebelik sürecinde anne vefetüs sağlığını olumsuz etkilemektedir. Çalışmamızda kronik hareketsizlikstresinin plasenta ve fetüs gelişimi üzerine etkilerini araştırmayı hedefledik.GEREÇ VE YÖNTEMLER: Balb/csuşu dişi fareler (20-30gr), 2dişi-1erkek olacak şekilde katıma alındı. Kontrolgrubundaki (n=6) gebe farelere herhangi bir uygulama yapılmazken, stresgrubundaki (n=6) gebe farelere gebeliğin 6.gününden 18.gününe kadar günde 3defa 45dakikalık kronik hareketsizlik stresine maruz bırakıldı. Gebeliğinin 18.Gününde plasenta ve fetüsler anestezi altında sezaryen ile alındı.BULGULAR: Prenatalstres, trofoblastik dev hücreler, glikojen içeren hücreler ve labirenttrofoblastik hücreler dahil olmak üzere birçok plasental hücrede apoptozuönemli ölçüde arttırdı ve intrauterin büyüme geriliğine sebep oldu. Stressüperoksit dismutaz ve glutatyon seviyelerini azalttı. Fetüsün gelişiminideğerlendirmek için, Alizarin Red S boyaması ile fetüsün kemikleşme merkezleri değerlendirildi.SONUÇ: Gebelik sürecindeki stres,apoptozu tetikleyerek, labirent bölgesi küçüldü ve plasenta yetmezliğine sebepoldu, ayrıca kollajen seviyelerini arttırarak fetüs gelişimini olumsuz yöndeetkileyerek intrauterin büyüme geriliği patogenezinde katkısı olduğunugözlemledik.
dc.description ABSTRACT AIM: Stress can affect negatively mother and fetuses duringpregnancy. We aimed to investigate the effects of chronic immobilization stresson 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 incontrol group (n=6) were left undisturbed, whereas pregnant mice in the stressgroup (n=6) were exposed to 45 min chronic immobilization stress for threetimes/day starting from gestational day 6 till 18. Fetuses and placentas wereremoved from dams on the gestational day 18 under anesthesia.RESULTS: The prenatal stress significantlyincreased apoptosis in several placental cells including trophoblastic giantcells, glycogen cells and labyrinth trophoblastic cells and resulted inintrauterine growth restriction. The stress caused a decreased superoxidedismutase and glutathione levels. Alizarin Red S staining shows theossification center of the fetuses to see developmental abnormality.CONCLUSION: Gestational stress causes placentaldysfunctions by triggering apoptosis, reducing the labyrinth zone as well asincreasing collagen levels, which may impair fetal development that maycontribute to pathogenesis of intrauterine growth restriction.
dc.format application/pdf
dc.language en
dc.publisher Süleyman Demirel Üniversitesi
dc.publisher Süleyman Demirel University
dc.relation https://dergipark.org.tr/tr/download/article-file/862347
dc.source Volume: 28, Issue: 1 31-39 en-US
dc.source 1300-7416
dc.source 2602-2109
dc.source SDÜ Tıp Fakültesi Dergisi
dc.subject Fetus,hareketsizlik stresi,plasenta
dc.subject fetus,immobilization stress,placenta
dc.title FARE GEBELİK DÖNEMİNDE HAREKETSİZLİK STRESİNİN PLASENTA VE YAVRUYA ETKİLERİ tr-TR
dc.title THE EFFECTS OF IMMOBILIZATION STRESS ON PLACENTA AND FETUS IN PREGNANT MICE en-US
dc.type info:eu-repo/semantics/article
dc.citation Referans1) Watson ED, Cross JC. Development of structures and transport functions in the mouse placenta, Physiology (Bethesda). 2005 Jun;20:180-93.
dc.citation 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
dc.citation 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.
dc.citation 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
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation Referans9) Demir R., İnsan plasentasında ışık mikroskobu, tarayıcı elektron mikroskobu bulguları ve ikizlerde perfüzyon incelemeleri, 1978.
dc.citation Referans10) Burtis C.A., Ashwood E.R., Tietz textbook of clinical chemistry, W.B. Saunders Company, Pennsylvania, 1994
dc.citation 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.
dc.citation 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.
dc.citation Referans13) Kaufmann P., Demonstration os cytoplasmic polyps from the human trophoblast by scanning electron microscopy, Arch. Gynakol. 211 (1970) 523.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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).
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation 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.
dc.citation Referans31) Yasemin Aksoy, The Role Of Glutathıone In Antıoxıdant Mechanısm, Turkiye Klinikleri J Med Sci. 2002;22(4):442-8.
dc.citation 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.
dc.citation Referans33) Erica D. Watson, James C. Cross, Development of Structures and Transport Functions in the Mouse Placenta, Physiology (Bethesda). 2005 Jun;20:180-93.


Files in this item

Files Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search DSpace


Advanced Search

Browse

My Account