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Archivos de Medicina de Urgencia de México

2024, Number 1

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Arch Med Urg Mex 2024; 16 (1)

Pathophysiology of placental preeclampsia

Cruz-Martínez FJ

Language: Spanish
References: 71
Page: 37-44
PDF size: 245.37 Kb.


ABSTRACT

Preeclampsia in general terms is a very interesting pathology from a pathophysiological point of view. In this article I will describe the pathophysiological mechanisms that participate in the development of placental preeclampsia, which is the first stage of several that lead to early-onset preeclampsia. I mention the participation of the multiple mechanisms that interact to cause the process of poor placentation. The participation of immunological and non-immunological components will be described, including macrophages, neutrophils, dendritic cells, natural killers, human leukocyte antigens, T lymphocytes (CD4, TH-17 and regulators), TH1/TH2 balance, endothelial dysfunction due to chronic-degenerative diseases, which participate in the altered remodeling of the uterine arteries that leads to uteroplacental hypoperfusion result in complex phenomena of apoptosis, necrosis and aponecrosis, which serve as a substrate for the secretion of microparticles that will be the triggers of the clinical manifestations in the mother.


REFERENCES

  1. Melchiorre K, Giorgione V, Thilaganathan. The placenta andpreeclampsia: villain or victim? Am J Obstet Gynecol. 2022 Feb; 226(2S):S954-S962. doi: 10.1016/j.ajog.2020.10.024.

  2. Roberts JM, Catov JM. Preeclampsia more than 1 disease: or isit? Hypertension. 2008 Apr;51(4):989-90. doi: 10.1161/HYPERTENSIONAHA.107.100248.

  3. Gonzáles-Merlo J, Gonzáles E, Fabre E. Obstetricia. Elseiver.2018.

  4. Christopher W. G. Redman, Ian L. Sargent. Inmunology ofPre-Eclampsia. American Journal of Reproductive Immunology2010; 63: 534-543.

  5. Robillard PY, Hulsey TC. Association of pregnancyinduced-hypertension,pre-eclampsia, and eclampsia with duration of sexual cohabitationbefore conception. Lancet 1996; 347: 619.

  6. Kho EM, McCowan LM, North RA, et al. On behalf of the SCOPEConsortium: duration of sexual relationship and its effect onpreeclampsia and small for gestational age perinatal outcome. JReprod Immunol 2009; 82: 66–73.

  7. Zhang J, Patel G: Partner change and perinatal outcomes. a systematicreview. Paediatr Perinat Epidemiol 2007; 21(1): 46–57.

  8. Basso O, Christensen K, Olsen J. Higher risk of Preeclampsia afterchange of partner. An effect of longer interpregnancy intervals?Epidemiology 2001; 12: 624–629.

  9. Tubbergen P, Lachmeijer AM, Althuisius SM, Vlak ME, van GeijnHP, Dekker GA. Change in paternity: a risk factor for preeclampsiain multiparous women? J Reprod Immunol 1999; 45: 81–88.

  10. Skjaerven R, Wilcox AJ, Lie RT. The interval between pregnanciesand the risk of preeclampsia. N Engl J Med 2002; 346: 33–38.

  11. Burton GJ, Jauniaux E. Placental oxidative stress: from miscarriageto preeclampsia. J Soc Gynecol Investig 2004; 11: 342–352.

  12. Wilczynski JR. Immunological analogy between allograft rejection,recurrent abortion and preeclampsia the same basic mechanism?Hum Immunol 2006; 67: 492–511.

  13. Billington WD. The immunological problem of pregnancy. 50 yearswith the hope of progress. A tribute to Peter Medawar. J ReprodImmunol 2003; 60: 1–11.

  14. Saito S, Sakai M, Sasaki Y, Nakashima A, Shiozaki A. inadequatetolerance induction may induce preeclampsia. J Reprod Immunol2007; 76: 30–39.

  15. Rajagopalan S, Long EO. Understanding how combinations ofHLA and KIR genes influence disease. J Exp Med 2005; 201:1025–1029.

  16. Hiby SE, Walker JJ, O’Shaughnessy KM, et al. Combinations ofmaternal KIR and fetal HLA-C genes influence the risk of preeclampsiaand reproductive success. J Exp Med 2004; 200: 957–965.

  17. Hiby SE, Regan L, Lo W, Farrell L, Carrington M, Moffett A. Associationof maternal killer-cell immunoglobulin-like receptors andparental HLA-C genotypes with recurrent miscarriage. Hum Reprod2008; 23: 972–976.

  18. Tilburgs T, Scherjon SA, van der Mast BJ, et al. Fetal-maternalHLA-C mismatch is associated with decidual T cell activation andinduction of functional T regulatory cells. J Reprod Immunol 2009;82: 148–157.

  19. Sun JC, Lanier LL. Natural killer cells remember: an evolutionarybridge between innate and adaptive immunity? Eur J Immunol

  20. 2009; 39: 2059–2064.20. Foster SL, Hargreaves DC, Medzhitov R. Gene-specific controlof inflammation by TLR-induced chromatin modifications. Nature2007; 447: 972–978.

  21. Mellor AL, Munn DH. Creating immune privilege. active local suppressionthat benefits friends, but protects foes. Nat Rev Immunol2008; 8: 74–80.

  22. Baban B, Chandler PR, Sharma MD, et al. IDO activates regulatoryT cells and blocks their conversion into Th17-like T cells. JImmunol 2009; 183: 2475–2483.

  23. Munn DH, Zhou M, Attwood JT, et al. Prevention of allogeneic fetalrejection by tryptophan catabolism. Science 1998; 281: 1191–1193.

  24. Nishizawa H, Hasegawa K, Suzuki M, et al. Mouse model forallogeneic immune reaction against fetus recapitulates humanpre-eclampsia. J Obstet Gynaecol Res 2008; 34: 1–6.

  25. Challis JR, Lockwood CJ, Myatt L, Norman JE, Strauss III JF,Petraglia F: Inflammation and pregnancy. Reprod Sci 2009; 16:206–215.

  26. Chaouat G. Regulation of T-cell activities at the fetoplacental interface—by placenta? Am J Reprod Immunol. 1999;42:199-204.

  27. Rustveld LO, Kelsey SF, Sharma R: Association between maternalinfections and preeclampsia: a systematic review of epidemiologicstudies. Matern Child Health J 2008; 12:223–242.

  28. Caretto D, Katzman SD, Villarino AV, Gallo E, Abbas AK: Cuttingedge: the Th1 response inhibits the generation of peripheral regulatoryT cells. J Immunol 2010; 184:30–34.

  29. Abrahams VM. Mechanisms of antiphospholipid antibody-associatedpregnancy complications. Thromb Res 2009; 124: 521–525.

  30. Dechend R, Muller DN, Wallukat G, Homuth V, Krause M, DudenhausenJ, et al. Activating autoantibodies against the AT1 receptorin preeclampsia. Autoimmun Rev 2005; 4: 61–65.

  31. Zhou CC, Zhang Y, Irani RA, et al. Angiotensin receptor agonisticautoantibodies induce pre-eclampsia in pregnant mice. Nat Med2008; 14: 855–862.

  32. Herse F, Verlohren S, Wenzel K, et al. Prevalence of agonisticautoantibodies against the angiotensin II type 1 receptor and solublefms-like tyrosine kinase 1 in a gestational age-matched casestudy. Hypertension 2009; 53: 393–398.

  33. Méndez JD, Xie J, Aguilar-Hernández M, Méndez-Valenzuela V.Trends in advanced glycation end products research in diabetesmellitus and its complications. Mol Cell Biochem 2010; 341: 33-41.

  34. Lahera V, Cediel E, de las Heras N, et al. Alteraciones del endotelioen la hipertensión 2003; 23(4): 3-12.

  35. Brosens IA, Robertson WB, Dixon HG. The role of the spiral arteriesin the pathogenesis of Preeclampsia. Obstet Gynecol Annu1972; 1: 177–191.

  36. Silasi M, Cohen B, Karumanchi SA, Rana S. Abnormal Placentation,Angiogenic Factors, and the Pathogenesis of PreeclampsiaObstet Gynecol Clin 2010; 37: 239–253.

  37. Ambreen A, Harrison A, Harrison M. Preeclampsia: Systemic EndothelialDamage Leading to Increased Activation of The BloodCoagulation Cascade. Journal of Biotech Research 2012; 4: 26-43

  38. Ortega MA, Fraile-Martínez O, García-Montero C, et al. The PivotalRole of the Placenta in Normal and Pathological Pregnancies:A Focus on Preeclampsia, Fetal Growth Restriction, and MaternalChronic Venous Disease. Cells. 2022 Feb 6;11(3):568. doi:10.3390/cells11030568.

  39. Ahn H, Park J, Gilman-Sachs A, Kwak-Kim J. Immunologic characteristicsof preeclampsia, a comprehensive review. Am JReprod Immunol. 2011 Apr;65(4):377-94. doi: 10.1111/j.1600-0897.2010.00913.x.

  40. Gebara N, Correia Y, Wang K, Bussolati B. Angiogenic Propertiesof Placenta-Derived Extracellular Vesicles in Normal Pregnancyand in Preeclampsia. Int J Mol Sci. 2021 May; 22(10): 5402. doi:10.3390/ijms22105402.

  41. Ferrara N. Vascular endothelial growth factor: basic science andclinical progress. Endocr Rev 2004; 25: 581–611.

  42. Nagy JA, Dvorak AM, Dvorak HF. VEGF-A (164/165) and PlGF:roles in angiogénesis and arteriogenesis. Trends Cardiovasc Med2003; 13(5): 169–175.

  43. Shibuya M, Claesson-Welsh L. Signal transduction by VEGF receptorsin regulation of angiogenesis and lymphangiogenesis. ExpCell Res 2006; 312(5): 549–560.

  44. Takahashi H, Shibuya M. The vascular endothelial growth factor(VEGF)/VEGF receptor system and its role under physiological andpathological conditions. Clin Sci (Lond) 2005; 109(3): 227–241.

  45. Maynard SE, Min JY, Merchan J, et al. Excess placental solublefms-like tyrosine kinase 1 (sFlt1) may contribute to endothelialdysfunction, hypertension, and proteinuria in preeclampsia. J ClinInvest 2003; 111(5): 649–658.

  46. Nagamatsu T, Fujii T, Kusumi M, et al. Cytotrophoblasts up-regulatesoluble fmslike tyrosine kinase-1 expression under reducedoxygen: an implication for the placental vascular developmentand the pathophysiology of preeclampsia. Endocrinology 2004;145(11): 4838–4845.

  47. Shore VH, Wang TH, Wang CL, et al. Vascular endothelial growthfactor, placenta growth factor and their receptors in isolated humantrophoblast. Placenta 1997; 18(8): 657–665.

  48. Gu Y, Lewis DF, Wang Y. Placental productions and expressions ofsoluble endoglin, soluble fms-like tyrosine kinase receptor-1, andplacental growth factor in normal and preeclamptic pregnancies. JClin Endocrinol Metab 2008; 93(1): 260–266.

  49. Sircar M, Thadhani R, Karumanchi SA. Pathogenesis of preeclampsia.Curr Opin Nephrol Hypertens. 2015 Mar;24(2):131-8.doi: 10.1097/MNH.0000000000000105.

  50. Gupta S, Agarwal A, Sharma R. The rol of placental oxidativestress and lipid peroxidation in preeclampsia. Obstet GynecolSurv 2005; 60: 807-816.

  51. Raijmakers M, Dechend R, Poston L. Oxidative stress and preeclampsia.rationale for antioxidant clinical trials. Hypertension2004; 44: 374-380.

  52. Lizarbe MI. El suicidio y la muerte celular. Revista de la Real Academiade Ciencias Exactas, Físicas y Naturales (Esp) 2007; 101: 1-33.

  53. Huppertz B, Herrler A. Regulation of proliferation and apoptosisduring development of the preimplantattion embryo and the placenta.Birth Def Res (part C) 2005;75:249-61.

  54. Majno G, Joris I. Apoptosis, oncosis, and necrosis. An overview ofcell death. Am J Pathol 1995; 146: 3-15.

  55. Lunetta P, Penttila A. Immunohistochemical identification of syncytiotrophoblasticcells and megakaryocytes in pulmonary vesselsin a fatal case of amniotic fluid embolism. Int J Legal Med 1996;108: 210-4.

  56. Huppertz B, Kadyrov M, Kigdom JC. Apoptosis and its role in thetrophoblast. Am J Obstet Gynecol 2006; 195: 29-39.

  57. 57 Knight M, Redman CW, Linton EA, Sargent IL. Shedding ofsyncytiotrophoblast microvilli into the maternal circulation inpre-eclamptic pregnancies. Br J Obstet Gynaecol 1998; 105(6):632-640.

  58. Johansen M, Redman CW, Wilkins T, Sargent IL. Trophoblast deportationin human pregnancy---its relevance for pre-eclampsia.Placenta1999; 20: 531-539.

  59. Formigli L, Papucci L, Tani A, et al. Aponecrosis: morphologicaland biochemical exploration of a syncretic process of cell deathsharing apoptosis and necrosis. J Cell Physiol 2000; 182: 41-49.

  60. Levy R, Smith SD, Chandler K, Sadovsky Y, Nelson DM. Apoptosisin human cultured trophoblasts is enhanced by hypoxia anddiminished by epidermal growth factor. Am J Physiol Cell Physiol2000; 278: C982-C988.

  61. Tjoa ML, Cindrova-Davies T, Spasic-Boskovic O, Bianchi DW,Burton GJ. Trophoblastic oxidative stress and the release of cell-free feto-placental DNA. Am J Pathol 2006; 169: 400-404.

  62. Straszewski S, Abrahams V, Mor G. The role of apoptosis in theregulation of trophoblast survival and differentiation during pregnancy.Endocrine Rev 2005; 26: 877-897.

  63. Smarason AK, Sargent IL, Starkey PM, Redman CW. The effect ofplacental syncytiotrophoblast microvillous membranes from normaland pre-eclamptic women on the growth of endotelial cells invitro. Br J Obstet Gynaecol 1993; 100: 943–949.

  64. Germain SJ, Sacks GP, Soorana SR, Sargent IL, Redman CW.Systemic inflammatory priming in normal pregnancy and preeclampsia:the role of circulating syncytiotrophoblast microparticles.J Immunol 2007; 178: 5949–5956.

  65. Sabapatha A, Gercel-Taylor C, Taylor DD. Specific isolation of placenta-derived exosomes from the circulation of pregnant womenand their immunoregulatory consequences. Am J Reprod Immunol2006; 56: 345–355.

  66. Vaughan JE, Walsh SW. Activation of NF-κB in Placentas of Womenwith Preeclampsia. Hypertens Pregnancy 2012; 31(2): 243–251.

  67. Seung SM, Romero R, Lee YJ, Park IS, Park CW, Bo Yoon BH.Systemic inflammatory stimulation by microparticles derived fromhypoxic trophoblast as a model for inflammatory response in Preeclampsia.American Journal of Obstetrics & Gynecology 2012;207: 337.e1-8.

  68. Echeverri NP, Mockus IS. Factor nuclear kB (NF-kB): Signalosomay su importancia en enfermedades inflamatorias y cáncer.Rev. Fac. Med 2008; 56 (2): 135.

  69. Nadeau-Vallée M, Obari D, Palacios J, et al. Sterile inflammationand pregnancy complications: a review. Reproduction. 2016 Dec;152(6):R277-R292. DOI: 10.1530/REP-16-0453.

  70. Schaefer L. Complexity of danger: the diverse nature of damage-associated molecular patterns. J Biol Chem. 2014 Dec19;289(51):35237-45. doi: 10.1074/jbc.R114.619304.

  71. Goulopoulou S, Davidge ST. Molecular mechanisms of maternalvascular dysfunction in preeclampsia. Send to Trends Mol Med.2015 Feb;21(2):88-97. doi: 10.1016/j.molmed.2014.11.009.




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