Placental apoptosis in pre-eclampsia

Ховхаева, П. А.; Krasnyi, Krasnyi A.M.; Тютюнник, Н. В.; Sergunina, Olga A.; Ганичкина, М. Б.; Амирасланов, Э. Ю.; Кан, Н. Е.; Тютюнник, В. Л.

doi:10.21518/2079-701x-2016-2-102-104

Cited by 4 publications

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“…Trophoblast apoptosis has been confirmed to occur in the placental tissue during pregnancy ( 25 ). The excessive apoptosis of placental trophoblasts leads to shallow implantation and the failure of uterine spiral artery reconstruction.…”

Section: Discussionmentioning

confidence: 99%

Fas regulates the apoptosis and migration of trophoblast cells by targeting NF‑κB

et al. 2021

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Placental trophoblast apoptosis is a major pathological feature of preeclampsia. Fas has been reported to be highly expressed in the placentas of patients with preeclampsia. However, the role and underlying mechanisms of Fas in the pathogenesis of preeclampsia have not been elucidated. In the present study, the expression of Fas in JAR human choriocarcinoma cells was overexpressed and knocked down to determine the function and possible mechanism of Fas in trophoblast cells in the progression of preeclampsia. The results of flow cytometry, Cell Counting Kit-8 and Transwell assays indicated that the overexpression of Fas promoted apoptosis, suppressed viability and impaired the migration of the human trophoblast cells. In addition, western blotting revealed that the overexpression of Fas increased the expression of nuclear factor kB (NF-kB), Bax, tumor necrosis factor α (TNF-α) and interleukin-2 (IL-2), and decreased the expression of Bcl-2 at the protein level in trophoblast cells. By contrast, the knockdown of Fas decreased the apoptosis of trophoblast cells and increased their viability and migration. In addition, the knockdown of Fas suppressed the expression of NF-κB, Bax, TNF-α and IL-2, and increased the expression of Bcl-2. Notably, the overexpression of NF-κB p65 attenuated the Fas knockdown-induced inhibition of apoptosis and acceleration of migration of the trophoblast cells. The overexpression of NF-κB in trophoblast cells also reversed the reduction in Bax expression and increase in Bcl-2 expression induced by Fas knockdown in trophoblast cells. These results indicate that Fas regulates the apoptosis and migration of trophoblast cells by targeting NF-κB, which suggests that the silencing of Fas is a promising therapeutic strategy for preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Fas regulates the apoptosis and migration of trophoblast cells by targeting NF‑κB

et al. 2021

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“…Destruction of these mechanisms in the trophoblast, stromal and endothelial cells of the villous chorion, decidual and amniotic membranes lead to changes in the placental-fetal interrelationships, and afterward -to the formation of placental insufficiency [2]. The processes of proliferation and apoptosis in the chorionic villi under the influence of various factors on the placenta are of great interest for scientists [2][3][4][5]. For example, at the Department of Pathological Anatomy of Bukovinian State Medical University in the context of the research work: "Improvement of pathological diagnosis of various forms of placental insufficiency" the determination of the lev-el of proliferative processes and processes of death in conditions of iron-deficiency anemia in gravidas (IDA) with impaired maturation of the chorionic tree in women who gave birth at 29-32 and 33-36 weeks of gestation is investigated 1 .…”

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confidence: 99%

Immunohistochemical Study of Trophoblasts Cellular Regulation Processes in Chorioamnionitis and Basal Deciduitis Combined with Iron-Deficiency Anemia in Gravidas

Ilika¹,

Garvasiuk²,

Іlika³

2021

Ukr. ž. med. bìol. sportu

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The purpose of the study is to establish quantitative parameters of cell proliferation and apoptosis in the trophoblast of the chorionic villi in chorioamnionitis and basal deciduitis combined with iron-deficiency anemia in gravidas by means of immunohistochemical method. Materials and methods. 198 placentas were examined. The immunohistochemical procedure was performed using primary antibodies against Ki-67 and Bax antigen with imaging by a polymer system with diaminobenzidine dye. The number of Ki-67-positive nuclei of the chorionic villi trophoblast was counted, and for the Bax antigen, the optical density of the immunohistochemical staining was measured by means of microdensitometric method. Comparison of differences in mean trends was performed using the odd Student’s two-sided t-test (p≤0.05). Results and discussion. The number of Ki-67-positive trophoblast nuclei in acute chorioamnionitis with iron-deficiency anemia in gravidas was 56±3.8 ‰, and the relative units of optical density of immunohistochemical staining for protein Bax – 0.234±0.0012, in chronic – 59±3.6 ‰ and 0.2, respectively. The number of Ki-67-positive nuclei of the chorionic villi trophoblast was counted. Placentas with acute as well as chronic chorioamnionitis and basal deciduitis showed even higher averages (p <0.001). In acute basal deciduitis in anemia, the number of Ki-67-positive trophoblast nuclei was 56±3.2 ‰, the average optical density of immunohistochemical staining for protein Bax – 0.236±0.0016, in chronic – 57±3.7 and 0.249±0.0015, respectively. It should be noted that in chronic chorioamnionitis and basal deciduitis, these rates were higher than in acute. With the same regularity the average indicators of optical density of immunohistochemical staining on protein Bax in a trophoblast of chorionic villi at comorbid iron-deficiency anemia concerning an inflammation without anemia increase. We have shown that proliferative activity in iron-deficiency anemia varies with gestational age and placental prematurity, but iron-deficiency anemia in gravidas and chorionic tree maturation both individually and in combination lead to the intensification of these processes. We obtained a justification for the arithmetic mean thickness and volume of the placenta relative to observations of placenta with inflammation without anemia in this comorbid pathology. Conclusion. Iron-deficiency anemia in gravidas leads to the intensification of proliferative processes and Bax-dependent apoptosis in the trophoblast of the chorionic villi of the placenta relative to the placenta from physiological pregnancy. In acute as well as in chronic chorioamnionitis and basal deciduitis, the proliferative activity and apoptotic processes in the trophoblast of the chorionic villi of the placenta increase, while comorbid iron-deficiency anemia in gravidas intensifies only the processes of Bax-dependent apoptosis

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Role of cytokines in pregnant women with chronic iron deficiency anemia in preeclampsia pathogenesis

K¹,

T²,

Da³

2020

OGIJ

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The frequency of development of hypertensive states in IDA reaches 32-45%. The pathogenesis of the combined complications of pregnancy with anemia and preeclampsia, including immunological aspects has been little studied. Purpose: to clarify the role of violations general and local cytokine status in pregnant women with anemia in the genesis of preeclampsia and justify the need to include immuno suppressants for the prevention and treatment of preeclampsia. Materials and methods: In 96 pregnant women with iron deficiency anemia (IDA) and preeclampsia in the third trimester of gestation the cytokine status of IL-1β, IL-6, IL-8, TNFα and lactoferrin in the serum of peripheral blood and in extracts of the placenta decidual tissue was examined by ELISA. Pregnant women were divided into 4 groups: 24-with mild anemia, 18-with moderate anemia, 26-with preeclampsia and with mild anemia and 28 pregnant women with preeclampsia and with moderate anemia. Results: It has been established that preeclampsia on the background of IDA is accompanied by a significant increase in the level of pro-inflammatory cytokines (p<0,05) and the acute phase protein lactoferrin (p<0,05) on the systemic and to a greater extent on the local level in the development of preeclampsia on the background of anemia of moderate severity (p<0,05). Discussion: The data obtained confirm the involvement of the immune system in the pathogenesis of preeclampsia, one of the trigger mechanisms of which is the immune imbalance in iron deficiency anemia. A pathogenetic rationale for the use of immunosuppressive therapy for combined pathology is given. Conclusion: The use of placental hormone - progesterone as an immunosuppressive drug in terms of substantiating new immunotherapy strategies for the prevention of preeclampsia is a topical trend in obstetric practice.

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Placental apoptosis in pre-eclampsia

Cited by 4 publications

References 10 publications

Fas regulates the apoptosis and migration of trophoblast cells by targeting NF‑κB

Fas regulates the apoptosis and migration of trophoblast cells by targeting NF‑κB

Immunohistochemical Study of Trophoblasts Cellular Regulation Processes in Chorioamnionitis and Basal Deciduitis Combined with Iron-Deficiency Anemia in Gravidas

Role of cytokines in pregnant women with chronic iron deficiency anemia in preeclampsia pathogenesis

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