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Decreased ALCAM expression and promoter hypermethylation is associated with preeclampsia.

Hypertens Res. 2020 Jan;43(1):13-22. Epub 2019 Oct 10
Li-Li Wei 1 , Yue-Shuai Pan 1 , Qian Tang 2 , Zong-Jun Yang 3 , Wei-Qing Song 4 , Yu-Fang Gao 1 , Jing Li 5 , Lu Zhang 6 , Shi-Guo Liu 7
Li-Li Wei 1 , Yue-Shuai Pan 1 , Qian Tang 2 , Zong-Jun Yang 3 , Wei-Qing Song 4 , Yu-Fang Gao 1 , Jing Li 5 , Lu Zhang 6 , Shi-Guo Liu 7
+ et al

[No authors listed]

Author information
  • 1 Department of Nursing, The Affiliated Hospital of Qingdao University, Qingdao, China.
  • 2 Prenatal Diagnosis Center, The Affiliated Hospital of Qingdao University, Qingdao, China.
  • 3 Department of Clinical Laboratory, Qingdao Women and Children's Hospital, Qingdao, China.
  • 4 Department of Clinical Laboratory, Qingdao Municipal Hospital, Qingdao, China.
  • 5 Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
  • 6 Prenatal Diagnosis Center, The Affiliated Hospital of Qingdao University, Qingdao, China. 0130aici@163.com.
  • 7 Prenatal Diagnosis Center, The Affiliated Hospital of Qingdao University, Qingdao, China. liushiguo2002@126.com.

摘要


Preeclampsia (PE) is a major obstetrical complication that results in maternal and fetal morbidity and mortality. Aberrant epigenetic modifications are widely involved in the pathogenesis of PE. Previously, the activated leukocyte cell adhesion molecule (ALCAM) was reported to be required for blastocyst implantation but has not been described in the context of pathological pregnancy. This study explored the expression of ALCAM and its methylation levels in the placentas and peripheral venous blood of patients with PE from a Chinese Han population. The mRNA and protein expression levels of ALCAM were downregulated in the PE placentas compared with the control placentas (P < 0.05). The methylation rate of the ALCAM gene promoter was considerably elevated in the placentas (P = 0.003, odds ratio (OR) = 0.264, 95% confidence interval (95% CI) [0.108-0.647], cases n = 47, controls n = 53) and peripheral blood (P = 0.007, OR = 0.455, 95% CI [0.256-0.806], cases n = 100, controls n = 100) of the PE patients compared with those of the normotensive women, suggesting a negative relationship between ALCAM methylation and gene transcription. Moreover, the transcriptional expression of ALCAM was dramatically increased by demethylating treatment in trophoblastic cells. ALCAM is expected to be involved in the pathogenesis of PE through methylation regulation.

KEYWORDS: Epigenetics, Methylation, Peripheral blood, Placenta, Preeclampsia