Association of –2548 G/A Polymorphism in the Leptin Gene with Preeclampsia/Pregnancy-Induced Hypertension

Sugathadasa, B. H. K. R.; Tennekoon, Kamani Hemamala; Karunanayake, E.H.; Kumarasiri, J. M.; Wijesundere, Anula

doi:10.3109/10641950903214617

Cited by 20 publications

(23 citation statements)

References 37 publications

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“…It is thought to arise due to abnormal placentation followed by a maternal systemic disorder. Several studies including ours have shown that PE/PIH is associated with elevated circulating leptin levels and reduced levels of soluble leptin receptor compared to normotensive pregnancies [11-14]. We previously demonstrated that a polymorphism in the leptin gene increases risk of PE/PIH [14].…”

Section: Resultsmentioning

confidence: 99%

LEPR c.668A>G polymorphism in a cohort of Sri Lankan women with pre-eclampsia / pregnancy induced hypertension: a case control study

et al. 2012

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BackgroundLeptin is known to be elevated in pre-eclampsia/ pregnancy induced hypertension (PE/PIH). However the reports on the association of leptin receptor (LEPR) c.668A>G polymorphism with PE/PIH are inconsistent.FindingsLEPR c.668A>G polymorphism was studied in a cohort of women with PE/PIH (N = 61) and normotensive pregnancies (N = 40) by polymerase chain reaction / restriction fragment length polymorphism. Genotype and allele frequencies were in Hardy-Weinberg equilibrium within both groups (Chi square test). Allele and genotype frequencies were not significantly different between PE/PIH and normotensive pregnancies (Chi square test). Leptin levels (Kruskal Wallis analysis of variance) and leptin/body mass index (one way analysis of variance) were not significantly different between genotypes within each group. However, leptin (Mann Whitney U test) and leptin normalised to body mass index (unpaired t test) were significantly higher in PE/PIH women homozygous and heterozygous for the G668 allele than in respective normotensives.ConclusionsWhether the leptin receptor c.668A>G polymorphism increases the risk of developing PE/PIH in Sri Lankan women remains inconclusive in view of the smaller sample studied. However leptin levels in PE/PIH appeared to be modulated by this polymorphism.

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Section: Resultsmentioning

confidence: 99%

LEPR c.668A>G polymorphism in a cohort of Sri Lankan women with pre-eclampsia / pregnancy induced hypertension: a case control study

et al. 2012

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“…Despite the intensive studies devoted to LEP gene expression, only some works have focused on the analysis of the hereditary variability of this gene and its role in changing the transcription level and the structure of susceptibility to pregnancy failure. It was shown that carriers of the AA genotype of the rs2167270 locus (G19A) located in the promoter region of the LEP gene have elevated levels of expression of this gene in the blood, as well as the risk of PE and hypertension [44]. Association between another polymorphism (G2548A) localized at the LEP gene promoter with gestational diabetes [45] was found in the Czech population.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Placental Tissue Transcriptome of Normal and Preeclampsia Complicated Pregnancies

et al. 2014

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Preeclampsia is one of the most severe gestational complications which is one of the leading causes of maternal and perinatal morbidity and mortality. A growth in the incidence of severe and combined forms of the pathology has been observed in recent years. According to modern concepts, inadequate cytotrophoblast invasion into the spiral arteries of the uterus and development of the ischemia-reperfusion syndrome in the placental tissue play the leading role in the development of preeclampsia, which is characterized by multipleorgan failure. In this regard, our work was aimed at studying the patterns of placental tissue transcriptome that are specific to females with PE and with physiological pregnancy, as well as identifying the potential promising biomarkers and molecular mechanisms of this pathology. We have identified 63 genes whose expression proved to differ significantly in the placental tissue of females with PE and with physiological pregnancy. A cluster of differentially expressed genes (DEG) whose expression level is increased in patients with preeclampsia includes not only the known candidate genes that have been identified in many other genome-wide studies (e.g., LEP, BHLHB2, SIGLEC6, RDH13, BCL6), but also new genes (ANKRD37, SYDE1, CYBA, ITGB2, etc.), which can be considered as new biological markers of preeclampsia and are of further interest. The results of a functional annotation of DEG show that the development of preeclampsia may be related to a stress response, immune processes, the regulation of cell-cell interactions, intracellular signaling cascades, etc. In addition, the features of the differential gene expression depending on preeclampsia severity were revealed. We have found evidence of the important role of the molecular mechanisms responsible for the failure of immunological tolerance and initiation of the pro-inflammatory cascade in the development of severe preeclampsia. The results obtained elaborate the concept of the pathophysiology of preeclampsia and contain the information necessary to work out measures for targeted therapy of this disease. ;

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“…These genes and proteins may be connected to atherosclerosis, diabetes, and Alzheimer's disease. In addition, Sugathadasa et al [39] showed that preeclampsia appears to be associated with the AA genotype of -2548 G/A polymorphism of the leptin gene. Genetic factors such as leptin gene polymorphism may increase the susceptibility of pregnant women to develop preeclampsia.…”

Section: Metabolic Systemmentioning

confidence: 99%

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

et al. 2011

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Association of –2548 G/A Polymorphism in the Leptin Gene with Preeclampsia/Pregnancy-Induced Hypertension

Abstract: Preeclampsia/pregnancy induced hypertension appears to be associated with higher circulating leptin and lower SLR levels, and with the AA genotype of −2548 G/A polymorphism of the leptin gene.

Cited by 20 publications

References 37 publications

LEPR c.668A>G polymorphism in a cohort of Sri Lankan women with pre-eclampsia / pregnancy induced hypertension: a case control study

LEPR c.668A>G polymorphism in a cohort of Sri Lankan women with pre-eclampsia / pregnancy induced hypertension: a case control study

Analysis of the Placental Tissue Transcriptome of Normal and Preeclampsia Complicated Pregnancies

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

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