Pre-Eclampsia PCR Array

先兆子痫PCR基因芯片 
 

Product	Species	Technology	Cat. No.
Pre-Eclampsia PCR Array	Human	Gene Expression	PAHS-163Z
Pre-Eclampsia PCR Array	Mouse	Gene Expression	PAMM-163Z
Pre-Eclampsia PCR Array	Rat	Gene Expression	PARN-163Z

Pre-Eclampsia RT² Profiler PCR Array profiles the expression of 84 key genes involved in dysregulation of placental development. Pre-eclampsia, a life-threatening disease, presents with high blood pressure during pregnancy, and delivery of the placenta provides the only cure. This disease is considered early-onset if the pregnancy is less than 32 weeks, and is otherwise called late-onset. The causes of pre-eclampsia are not entirely understood. Many patients show poor placental implantation, suggesting that pre-eclampsia begins very early in pregnancy, even though the symptoms only arise later. A potential molecular mechanism involves defective vascular remodeling by trophoblasts early in placental development. As the disease progresses, the placenta may become hypoxic, causing inflammation and oxidative stress. These processes result in the infiltration of immune cells such as T helper 1 (Th1) cells, neutrophils, and natural killer cells. A similar process results in intrauterine growth retardation, or insufficient fetal growth. Active areas of pre-eclampsia research include the effort to identify women with a high risk of pre-eclampsia during their pregnancy. In addition, research determining the key genes involved in pre-eclampsia may lead to novel therapeutic targets to inhibit or reverse the condition. Using real-time PCR, research studies can easily and reliably analyze the expression of a focused panel of genes involved in pre-eclampsia with this array.
先兆子痫PCR基因芯片可以同时检测影响胎盘发育失调的84个关键基因的表达。先兆子痫，是一种危及生命的疾病，主要表现为怀孕期间的高血压，胎盘的分娩是现有的唯一的治疗方法。这种疾病发生在孕期小于32周被称为早期，超过32周则被称为迟发性。先兆子痫的原因现在不完全清楚。许多患者会出现胎盘植入的失败，这一现象提示我们虽然病征出现很晚，但可能在更早期先兆子痫就有了影响。一个潜在的分子机制涉及到滋养细胞早期胎盘发育的血管重塑缺陷。随着病情的发展，胎盘缺氧，引起炎症和氧化应激。这些过程导致的免疫细胞（如Th1细胞，中性粒细胞和自然杀伤细胞）的浸润。类似的过程会导致胎儿宫内发育迟缓，或胎儿的生长发育不足。先兆子痫主要的研究方向集中在明确妇女在怀孕期间是否产生先兆子痫的高风险。此外，研究还涉及明确先兆子痫的关键基因及新的治疗靶点，抑制或逆转的条件。利用实时定量PCR，研究者可以方便并且可信地对先兆子痫相关基因进行同时检测。
Placental Genes Dysregulated During Pre-eclampsia:
Early-Onset: ABCG2 (BCRP), ANGPT2, ATP1B1, BCL6, BHLHE40, CFD, COL14A1, CRH, DCN, DUSP1, F5, FABP4, FLT1 (VEGFR1), FSTL3, HGF, HSD17B1, HTRA1, IGF1, INHA, INHBA, LEP, LPL, MMP12, SOD1, SPP1, VCAN.
Late-Onset: ABCC1 (MRP1), ABCG2, APLN, ATP2A2, BCL6, BHLHE40, C3, CAV1, CD40LG (TNFSF5), CDH13, CLU, CP, CRH, CRHBP, CXCL9, CYP26A1, DUSP1 (PTPN16), F5, FLT1, FSTL3, HBEGF (DTR), HP, HSD17B1, HSP90AA1, HTR3A, HTRA1, IFNG, IGFBP3, IL11, IL15, IL1A, INHA, INHBA, ITGB3, KIT (CD117), KRT19, LEP, MAS1, NCAM1, NDRG1, NTRK2, PDGFD, PGR, QPCT, SERPINA3, SOD1, SPP1, STAT1, TAC1, TGFB1, TREM1.
Genes Involved in Pregnancy:
Pregnancy Maintenance: ADM, ANGPT2, CRH, CRHBP, DCN, FLT1 (VEGFR1), HIF1A, HLA-G, IL11, KRT19, LEP, PGF, PGR, SOD1, TAC3, TGFB1.
Angiogenesis: ANGPT2, C3, CCL2 (MCP-1), CDH13, CXCL10 (INP10), DCN, ENG (EVI-1), FLT1 (VEGFR1), FLT4 (VEGFR2), HIF1A, IL18, IL1A, IL6, IL8, ITGB3, MMP9, NDRG1, NOS3 (eNOS), PGF, TEK (TIE2), VEGFA.
Vasodilation: ADM, AGTR1, APLN, MAS1, NOS3 (eNOS).
Tissue Remodeling: MMP9, MMP12, PAPPA2, SERPINA3.
Inflammation: AGTR1, BCL6, C3, CCL2 (MCP-1), CD40LG (TNFSF5), CRH, CXCL10 (INP10), CXCL9 (MIG), FABP4, IL10, IL15, IL18, IL1A, IL2, IL6, IL8, SERPINA3, SPP1, TAC1, TGFB1, TNF.
Oxidative Stress: CLU, CYP26A1, DUSP1 (PTPN16), HIF1A, MMP9, SOD1.
Adhesion: CAV1, CD40LG (TNFSF5), CDH13, COL14A1, ENG (EVI-1), FSTL3, ITGB3, NCAM1, SPP1, VCAN.
Cells Involved in Pre-eclampsia:
Th1 Cells: CD40LG (TNFSF5), IFNG, IL18, IL2, STAT1, TNF, VEGFA.
Endothelial Cells: ANGPT2, CAV1, CCL2 (MCP-1), CD40LG (TNFSF5), CDH13, EDN1, FLT4 (VEGFR2), HIF1A, ITGB3, NOS3 (eNOS), TEK (TIE2), TGFB1, VEGFA.
Neutrophils: CCL2 (MCP-1), EDN1, IFNG, IL6, IL8, TREM1.
Natural Killer Cells: IL2, IL15, IL18.
Hemostasis & Heme Metabolism: ABCG2 (BCRP), ATP1B1, ATP2A2, C3, CFD, CYP26A1, F5, HP, INHA, INHBA.
Hormones & Growth Factors: ADM, APLN, CRH, CRHBP, EDN1, HBEGF (DTR), HGF, IGF1, INHA, INHBA, LEP, PDGFD, PGF, QPCT, TAC1, TAC3.
Signal Transduction:
Nitric Oxide Signaling: CAV1, EDN1, ENG (EVI-1), HSP90AA1, NOS3 (eNOS).
Insulin Signaling: HTRA1, IGF1, IGFBP3.