Immunohistochemical expression of Annexin A5 in preeclamptic placentas☆

Ornaghi, Sara; Vergani, Patrizia; Urban, G.; Giardini, Valentina; Moltrasio, Francesca; Leone, Biagio Eugenio

doi:10.1016/j.placenta.2010.12.015

Cited by 18 publications

(16 citation statements)

References 28 publications

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“…The majority PE samples exhibited signi cantly lower ANXA5 mRNA levels compared to controls, however, the difference was little in mRNA expression between the early-onset and late-onset groups. Reduced ANXA5 mRNA and protein has been also reported in previous studies that assessed the placental expression of ANXA5 in women with PE 17,18 , and has been correlated…”

Section: Discussionsupporting

confidence: 70%

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Expression of Annexin A5 in maternal blood and placenta in pregnancies with preeclampsia

Teng¹,

Yu²,

Pan³

et al. 2022

Preprint

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Background The placental anticoagulant protein Annexin A5 is highly expressed on the apical surfaces of syncytiotrophoblasts and plays an important role in maintaining blood fluidity in the placental circulation. We investigated the expression of Annexin A5 in maternal blood and placentas from pregnancies complicated by preeclampsia compared with uncomplicated pregnancies. Materials and Methods Placental tissue and maternal blood were collected from pregnancies complicated by preeclampsia. They were classified into two groups: early-onset group (n = 10), late-onset group (n = 10) .10 women without perinatal complications who accepted elective term cesarean section were chosen as the control group. Western blot and immunohistochemistry were used to detect the expression and localization of Annexin A5 in the placenta. Annexin A5 mRNA expression was quantified by Real-Time PCR. Annexin A5 and coagulation factor Xa in maternal blood was measured by an enzyme-linked immunosorbent assay. Prothrombin time, activated partial thromboplastin time, Thrombin time, fibrinogen were detected in each groups. Results (1) The expression of Annexin A5 in maternal blood were: 5.54±0.29 in early-onset group; 5.10±0.28 in late-onset group; 4.5±0.19 in control group. They were significantly higher in preeclampsia groups than in control group (P = 0.013). However, there was no significant difference among preeclampsia groups (P > 0.05). The mean ±SD coagulation factor Xa expression in the early-onset and late-onset group were 1229.23±45.33 and 1366.96±56.30 versus 1372.95±45.44 in the control group, which has not statistically significant(P=0.072). (2) The protein expression of Annexin A5 in placenta was not statistically significant between the early-onset, late-onset, and control groups (mean ± SD): 0.01 ± 0.02, 0.95±0.03vs.0.99 ± 0.02, p = 0.071.(3) The Annexin A5 mRNA levels in placenta were: 0.79±0.23 in early-onset group; 1.18±0.53 in late-onset group; respectively. All were significantly lower than that in control group (6.19±1.68, P =0.024), and no significant difference was found among preeclampsia groups (P > 0.05). (4) Prothrombin time, activated partial thromboplastin time, Thrombin time, fibrinogen levels were: (11.9 ± 0.23), (33.38± 0.85) s, (16.88 ± 0.45) g/L and 3.85 ± 0.23 in early-onset group; (11.65 ± 0.12), (33.15 ± 0.36) s, (16.13 ± 0.19) g/L and 4.91 ± 0.14 in late-onset group; (12.01 ± 0.09), (32.08 ± 0.41) s, (16.34 ± 0.24) g/L and 4.32 ± 0.20 in control group. The first three were no significant difference among preeclampsia groups and control group (P > 0.05), fibrinogen was statistically significant among all groups (P < 0.05). Conclusion These results suggest that Annexin A5 plays an important role in the pathogenesis and progression of preeclampsia by affecting coagulation.

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Section: Discussionsupporting

confidence: 70%

“…with disease onset and the presence of FGR 17,19 . However, Ornaghi et al 17 using the immunohistochemical Tissue Microarray (TMA) technique found ANXA5 expression to be related only to FGR but not to PE or its clinical severity.…”

Section: Discussionmentioning

confidence: 99%

Expression of Annexin A5 in maternal blood and placenta in pregnancies with preeclampsia

Teng¹,

Yu²,

Pan³

et al. 2022

Preprint

View full text Add to dashboard Cite

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“…Therefore, defining the gene expression of preeclamptic placentas has been the focus of numerous studies (Damiano, 2011;Ornaghi et al, 2011;Shin et al, 2011;Wang et al, 2011). To our knowledge, a number of comprehensive analyses have been conducted on the gene expression in preeclamptic placentas using DNA microarrays Pang and Xing, 2003a, 2003b, 2004Reimer et al, 2002;Sitras et al, 2009;Tsoi et al, 2003;Zhou et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Identification of Differential Gene Expression Profiles in Placentas from Preeclamptic Pregnancies Versus Normal Pregnancies by DNA Microarrays

Meng

Chen

Sun

et al. 2012

OMICS: A Journal of Integrative Biology

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The purpose of this study was to perform a comprehensive analysis of gene expression profiles in placentas from preeclamptic pregnancies versus normal placentas. Placental tissues were obtained immediately after delivery from women with normal pregnancies (n = 6) and patients with preeclampsia (n = 6). The gene expression profile was assessed by oligonucleotide-based DNA microarrays and validated by quantitative real-time RT-PCR. Functional relationships and canonical pathways/networks of differentially-expressed genes were evaluated by GeneSpring Ô GX 11.0 software, and ingenuity pathways analysis (IPA). A total of 939 genes were identified that differed significantly in expression: 483 genes were upregulated and 456 genes were downregulated in preeclamptic placentas compared with normal placentas (fold change ‡ 2 and p < 0.05 by unpaired t-test corrected with Bonferroni multiple testing). The IPA revealed that the primary molecular functions of these genes are involved in cellular function and maintenance, cellular development, cell signaling, and lipid metabolism. Pathway analysis provided evidence that a number of biological pathways, including Notch, Wnt, NF-jB, and transforming growth factor-b (TGF-b) signaling pathways, were aberrantly regulated in preeclampsia. In conclusion, our microarray analysis represents a comprehensive list of placental gene expression profiles and various dysregulated signaling pathways that are altered in preeclampsia. These observations may provide the basis for developing novel predictive, diagnostic, and prognostic biomarkers of preeclampsia to improve reproductive outcomes and reduce the risk for subsequent cardiovascular disease.

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“…We have recently demonstrated that the enzyme HtrA1, involved in the physiological development of many organs, is differentially regulated in PE-AGA and PE-FGR placentas [24] as well as the transcription factors JunD and c-jun, implicated in regulating cytotrophoblast proliferation and differentiation, showing an opposite modulation in PE-AGA and PE-FGR [25]. Moreover, Ornaghi and colleagues observed that placental expression of anticoagulant protein Annexin 5 was significantly lower only in PE complicated by FGR—but not in PE-AGA—compared to controls [26]. Often in the literature “placental PE” and “maternal PE” are used as synonymous of “early onset” or “severe” PE and “late onset” or “mild” PE, respectively.…”

Section: Discussionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction

Cardaropoli

Paulesu

Romagnoli

et al. 2012

Clinical and Developmental Immunology

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The proinflammatory cytokine MIF (macrophage migration inhibitory factor) is involved in physiological and pathological processes in pregnancy. MIF maternal serum levels are increased in preeclampsia (PE). We hypothesize that pregnancy tissues are the source of MIF overexpression in PE. MIF protein was studied in maternal sera, placental tissues, fetal membranes, and umbilical cord of 8 control and 20 PE pregnancies: 10 with normal fetal growth (PE-AGA) and 10 with fetal growth restriction (PE-FGR). MIF levels were significantly higher in PE-AGA membranes than in controls and PE-FGR. In PE-FGR, MIF cord concentrations were higher than in PE-AGA while MIF placental levels were lower than in controls. MIF maternal serum levels were higher in PE, compared to controls, and the difference was mainly due to PE-FGR samples. These data support MIF involvement in PE pathogenesis and suggest that different pregnancy tissues contribute to MIF production in PE with and without fetoplacental compromise.

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Immunohistochemical expression of Annexin A5 in preeclamptic placentas☆

Cited by 18 publications

References 28 publications

Expression of Annexin A5 in maternal blood and placenta in pregnancies with preeclampsia

Expression of Annexin A5 in maternal blood and placenta in pregnancies with preeclampsia

Identification of Differential Gene Expression Profiles in Placentas from Preeclamptic Pregnancies Versus Normal Pregnancies by DNA Microarrays

Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction

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