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Novel Biomarkers for Predicting Preeclampsia

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Novel Biomarkers for Predicting Preeclampsia Rabbany SY, Heissig B, Hattori K & Rafii S: Urbich C & Dimmeler S: 2004. Endo- modulates signaling from the G-CSF recep- 2003. Molecular pathways regulating mobi- thelial progenitor cells functional char- tor. Leukemia 14:1284–1291. lization of marrow-derived stem cells for acterization. Trends Cardiovasc Med 14: You-Ten KE, Muise ES, Itie A, et al.: 1997. – tissue revascularization. Trends Mol Med 9: 318 322. Impaired bone marrow microenvironment – 109 117. Vercauteren M, Remy E, Devaux C, et al.: 2006. and immune function in T cell protein Ribatti D: 2008. Hemangioblast does exist. Improvement of peripheral endothelial dys- tyrosine phosphatase-deficient mice. J Exp Leuk Res 32:850–854. function by protein tyrosine phosphatase Med 186:683–693. inhibitors in heart failure. Circulation 114: Salmond RJ & Alexander DR: 2006. SHP2 YuM,LuoJ,YangW,etal.:2006.The 2498–2507. forecast for the immune system: fog gra- scaffolding adapter Gab2, via Shp-2, reg- dually clearing. Trends Immunol 27: Walter DH, Haendeler J, Reinhold J, et al.: ulates kit-evoked mast cell proliferation by 154–160. 2005. Impaired CXCR4 signaling contri- activating the Rac/JNK pathway. J Biol butes to the reduced neovascularization Chem 281:28615–28626. Seki Y, Kai H, Shibata R, et al.: 2000. Role of capacity of endothelial progenitor cells the JAK/STAT pathway in rat carotid artery from patients with coronary artery disease. remodeling after vascular injury. Circ Res Circ Res 97:1142–1151. 87:12–18. Ward AC, Oomen SP, Smith L, et al.: 2000. The Sharlow ER, Pacifici R, Crouse J, et al.: 1997. SH2 domain-containing protein tyrosine Hematopoietic cell phosphatase negatively phosphatase SHP-1 is induced by granulo- regulates erythropoietin-induced hemoglo- cyte colony-stimulating factor (G-CSF) and PII S1050-1738(08)00101-1 TCM binization in erythroleukemic SKT6 cells. Blood 90:2175–2187. Shepherd RM, Capoccia BJ, Devine SM, et al.: 2006. Angiogenic cells can be rapidly mobi- lized and efficiently harvested from the blood following treatment with AMD3100. Blood 108:3662–3667. Simoncic PD, Bourdeau A, Lee-Loy A, et al.: 2006. T-cell protein tyrosine phosphatase (Tcptp) is a negative regulator of colony- Novel Biomarkers for Predicting stimulating factor 1 signaling and macro- phage differentiation. Mol Cell Biol 26: Preeclampsia – 4149 4160. David M. Carty, Christian Delles, and Anna F. Dominiczak⁎ Socinski MA, Cannistra SA, Elias A, et al.: 1988. Granulocyte–macrophage colony sti- mulating factor expands the circulating haemopoietic progenitor cell compartment in man. Lancet 1:1194–1198. Preeclampsia is a major cause of maternal morbidity and mortality Sugano M, Tsuchida K, Maeda T & Makino N: worldwide. Despite decades of research into the condition, the ability of 2007. SiRNA targeting SHP-1 accelerates clinicians to predict preeclampsia prior to the onset of symptoms has not angiogenesis in a rat model of hindlimb improved significantly. In this review, we will examine the pathophysiol- ischemia. Atherosclerosis 191:33–39. ogy underlying preeclampsia and will look at potential biomarkers for Takahashi T, Kalka C, Masuda H, et al.: 1999. Ischemia- and cytokine-induced mobiliza- early prediction and diagnosis. In addition, we will explore potential tion of bone marrow-derived endothelial future areas of research into the condition. (Trends Cardiovasc Med progenitor cells for neovascularization. Nat – n Med 5:434–438. 2008;18:186 194) 2008, Elsevier Inc. Tan Y, Shao H, Eton D, et al.: 2007. Stromal cell-derived factor-1 enhances pro-angio- Introduction a major cause of maternal morbidity and genic effect of granulocyte-colony stimulat- mortality worldwide. The cardinal clin- ing factor. Cardiovasc Res 73:823–832. Preeclampsia is a multisystem disorder ical features of the condition are hyper- of pregnancy, which complicates 3%-5% Thum T, Hoeber S, Froese S, et al.: 2007. Age- tension and proteinuria occurring after dependent impairment of endothelial pro- of pregnancies in the western world. It is genitor cells is corrected by growth-hor- 20 weeks gestation in women who were mone-mediated increase of insulin-like not previously known to be hypertensive. growth-factor-1. Circ Res 100:434–443. Other signs and symptoms include David M. Carty, Christian Delles, and Anna F. edema and headache, and in severe Tsui FW, Martin A, Wang J & Tsui HW: 2006. Dominiczak are at the BHF Glasgow Cardio- Investigations into the regulation and func- vascular Research Centre, University of Glas- cases, the condition is associated with tion of the SH2 domain-containing protein- gow, G12 8TA Glasgow, United Kingdom. seizures (eclampsia), liver, and kidney tyrosine phosphatase, SHP-1. Immunol Res ⁎ Address correspondence to: Prof. Anna F. dysfunction as well as clotting abnorm- – 35:127 136. Dominiczak, BHF Glasgow Cardiovascular alities, Adult Respiratory Distress Syn- Urbich C, Aicher A, Heeschen C, et al.: 2005. Research Centre, University of Glasgow, 126 drome and fetal growth restriction (FGR) Soluble factors released by endothelial University Place, G12 8TA Glasgow, United (Davison et al. 2004). progenitor cells promote migration of Kingdom. Tel.: (+44) 141 330 5420; fax: (+44) endothelial cells and cardiac resident pro- 141 330 6997; e-mail: [email protected]. The cause of preeclampsia remains genitor cells. J Mol Cell Cardiol 39: © 2008 Elsevier Inc. All rights reserved. unknown, and the only known cure is 733–742. 1050-1738/08/$-see front matter delivery of the fetus and placenta. 186 TCM Vol. 18, No. 5, 2008 Various agents have been evaluated to The imaging technique that has so far ments of the spiral arteries, at around 10- see whether they influence the develop- been most widely used for predicting 12 weeks gestation; the second involves ment of preeclampsia. Aspirin has been preeclampsia has been uteroplacental invasion of the myometrial segments at studied extensively; it was summarized Doppler ultrasound. Impaired placental 15-16 weeks (Sargent and Smarason in a Cochrane review by Duley et al. perfusion, one of the hallmarks of pre- 1995). In preeclampsia, the cytotropho- (2004) to have modest but significant eclampsia, can be assessed by measuring blastic invasion of the myometrial seg- benefits in preventing preeclampsia. It is flow waveform ratios or by detecting ments is impaired: the spiral arteries commonly used in women who are diastolic notching of the uterine arcuate remain narrow, and blood supply to the known on the basis of risk factors to be vessels. Uterine Doppler studies can, fetus is restricted. The effects of this on at high risk of developing preeclampsia, however, be inconsistent: different types the fetus become more significant as although questions remain over exactly of machine, different gestational age at pregnancy progresses, since the uterine which subgroups of women are most assessment, and different definitions of vasculature is unable to keep up with the likely to benefit. Studies of calcium abnormal flow velocity waveforms make increased amount of blood and nutrients supplementation suggest that it is of accurate comparison of studies difficult. necessary for fetal development. Placen- most benefit when used in high-risk A large systematic review of 43 studies tal ischemia is thought to develop as a women with low dietary calcium intake involving 40,000 patients (Conde-Agu- result of this abnormal cytotrophoblastic (Hofmeyr et al. 2006), although studies of delo et al. 2004) found that, in both low- invasion; this has been proposed as antioxidants such as vitamins C and E and high-risk patient groups, the positive leading to release of placental factors and magnesium and zinc supplements predictive value was not sufficiently high and imbalance of angiogenic factors, have been less promising (Poston et al. to recommend routine screening. causing the widespread endothelial dys- 2006). Attention has therefore turned in function which characterizes preeclamp- Despite decades of research into the recent years towards identifying mater- sia (Lee et al. 2007). condition, predicting which women are at nal markers of placental dysfunction increased risk of developing preeclampsia which are raised in women who go on Angiogenic factors remains problematic. Identifying “at-risk” to develop preeclampsia. In this review, women is an important aim; because we will look at novel biomarkers which As research in the field of preeclampsia modern obstetric care places emphasis have been used in the prediction of progresses, much of the attention in upon the primary care setting for expec- preeclampsia and explore potential recent years has been focused on peptides tant women, a marker which identified future areas of investigation. related to angiogenesis. Angiogenesis, the high-risk women would allow for closer development of new blood vessels from supervision in secondary care. Such a existing endothelium, is essential for Pathogenesis of preeclampsia marker would also facilitate recruitment normal placental development. Two of for trials of potential therapeutic agents, Although the cause of preeclampsia the angiogenic growth factors, vascular for accurate diagnosis, and for timely remains elusive, the origin of the condi- endothelial growth factor (VEGF) and intervention whenever problems develop. tion is recognized as lying in the placenta. placental growth factor (PlGF) are Furthermore, predicting preeclampsia in This is known to be the case because thought to contribute to normal tropho- women with underlying conditions such preeclampsia
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