Expression of TGF-β1 and miR-99a in serum of patients with early spontaneous abortion and correlation with hormone levels during pregnancy

Xie, Juping; Cao, Yali

doi:10.3892/etm.2019.7477

Cited by 7 publications

(7 citation statements)

References 19 publications

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“…One study indicated that miR-99a could be linked to long-term estrogen deprivation [31]. One clinical study indicated that progesterone and estrogen were negatively correlated with the expression level of miR-99a [32]. Thus, we speculated that miR-99a could be related to menopausal depression.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-99a is a Potential Target for Regulating Hypothalamic Synaptic Plasticity in the Peri/Postmenopausal Depression Model

Yang

Zhang

Cao

et al. 2019

Cells

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Accumulating evidence has demonstrated that there is a growing trend of menopausal women suffering from depression. However, the pathogenesis of menopausal depression still remains unclear. Hence, this paper aims to reveal the pathological mechanisms involved in postmenopausal depression by using a novel peri-to postmenopausal depression model induced by a two-step ovariectomy plus chronic mild stress (CMS). The results of metabolic chambers and serum hormone/cytokine determination revealed that peri/postmenopausal depressive mice exhibited endocrine and metabolic disorders. Electrophysiological recordings indicated that the hippocampal synaptic transmission was compromised. Compared to the sham group, the microRNA-99a (miR-99a) level decreased significantly in the hypothalamus, and its target FK506-binding protein 51 (FKBP51) enormously increased; in contrast, the nuclear translocation of the progesterone receptor (PR) decreased in hypothalamic paraventricular nucleus (PVN) in the peri/postmenopausal depression mouse model. Additionally, synaptic proteins, including postsynaptic density protein 95 (PSD-95) and synaptophysin (SYN), showed a similar decrease in the hypothalamus. Accordingly, the present work suggests that miR-99a may be involved in the regulation of hypothalamic synaptic plasticity and that it might be a potential therapeutic target for peri/postmenopausal depression. relieves symptoms in some patients: estrogen administered along with antidepressants [8] could give rise to detrimental effects [9,10]. Due to the lack of clarity in the current forms of treatment, there is an urgent need to determine the underlying pathogenesis of menopausal depression and to identify new therapeutic drugs.There is a strong association between depression and metabolic syndrome. The nervous and endocrine systems orchestrate adaptive responses to stressful stimuli involving behavioral, emotional, and metabolic alterations [11]. Metabolic disorders, such as obesity and diabetes, are associated with elevated rates of depression [12]. Depression is often associated with increased hypothalamic-pituitary-adrenal (HPA) axis activity and increased levels of glucocorticoids. In particular, increased levels of circulating proinflammatory cytokines and concomitant inflammation activation such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) in the brain and blood can lead to depressive symptoms. Several studies have revealed that repeated environmental or psychosocial stress gives rise to synaptic plasticity deficits and neurotransmitter dysregulation, resulting in depressive-like behavior [13].Synaptic plasticity, one of the most fundamental brain functions, has recently been found to be an indispensable target in treating depression [14]. Mounting evidence has suggested that stress has profound effects on synaptic forms and functions [15]. Synaptic plasticity includes both structure and transmission plasticity. Studies have indicated that postsynaptic density (PSD) molecules, such as PSD-95, ar...

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Section: Resultsmentioning

confidence: 99%

MicroRNA-99a is a Potential Target for Regulating Hypothalamic Synaptic Plasticity in the Peri/Postmenopausal Depression Model

Yang

Zhang

Cao

et al. 2019

Cells

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“…In the present study, serum samples but not plasma samples were used, as plasma contains fibrinogen, which may affect certain proteinsindicators (29). In numerous studies of the roles of ncRNAs in the human circulation, serum samples may better reflect the exact differential expression of these RNAs in various pathologicalsstates (30)(31)(32). Furthermore, the blood samples were all centrifuged for serum isolation immediately after collection to avoid hemolysis in this experiment.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of lncRNA SNHG1/miR‑145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis

Dong

2021

Exp Ther Med

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Carotid angioplasty and stenting have developed into reliable options for patients with carotid stenosis. However, postoperative restenosis remains a serious and unresolved problem. Restenosis is partly caused by the proliferation of vascular smooth muscle cells. As certain long non-coding RNAs (lncRNAs) affect cell proliferation and migration, the present study aimed to investigate them as novel biomarkers for restenosis development and to further reveal the potential underlying mechanisms. The expression of lncRNA small nucleolar RNA host gene 1 (SNHG1) and microRNA145 (miR-145) in human carotid artery smooth muscle cells (hHCtASMCs) was analyzed using reverse transcription-quantitative PCR. In addition, a luciferase reporter assay was performed to investigate the interaction between SNHG1 and miR-145. The effects of the SNHG1/miR-145 axis on the proliferation and migration of hHCtASMCs were evaluated by Cell Counting Kit-8 and Transwell assays. Serum SNHG1 and miR-145 expression levels were increased and decreased, respectively, in patients with restenosis (all P<0.001). High SNHG1 and low miR-145 were identified as risk factors for restenosis onset (all P<0.01). Furthermore, decreasing SNHG1 expression levels in hHCtASMCs inhibited cell proliferation and migration. The luciferase reporter assay and expression results demonstrated that miR-145 may be a target of SNHG1 and mediated the effects of SNHG1 on hHCtASMC proliferation and migration. The results obtained suggested that abnormal expression of SNHG1 and miR-145 may be risk factors for restenosis. The present study revealed that the SNHG1/miR-145 axis regulates hHCtASMC proliferation and migration, indicating its potential for restenosis prevention and treatment.

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“…In humans, TGF-β serum levels are elevated in pregnant women compared to non-pregnant women, and serum levels are higher in early pregnancy compared to late pregnancy (123). However, women experiencing RPL display a decrease in TGF-β serum levels compared to women undergoing elective termination for non-medical reasons (124). Interestingly, there are indications from mouse studies that TGFβ induced Tregs could prevent spontaneous abortion, but this effect needs to be elucidated further (111,125).…”

Section: Tgf-βmentioning

confidence: 99%

Regulatory T Cells in Pregnancy: It Is Not All About FoxP3

et al. 2020

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In pregnancy, the semi-allogeneic fetus needs to be tolerated by the mother's immune system. Regulatory T cells (Tregs) play a prominent role in this process. Novel technologies allow for in-depth phenotyping of previously unidentified immune cell subsets, which has resulted in the appreciation of a vast heterogeneity of Treg subsets. Similar to other immunological events, there appears to be great diversity within the Treg population during pregnancy, both at the maternal-fetal interface as in the peripheral blood. Different Treg subsets have distinct phenotypes and various ways of functioning. Furthermore, the frequency of individual Treg subsets varies throughout gestation and is altered in aberrant pregnancies. This suggests that distinct Treg subsets play a role at different time points of gestation and that their role in maintaining healthy pregnancy is crucial, as reflected for instance by their reduced frequency in women with recurrent pregnancy loss. Since pregnancy is essential for the existence of mankind, multiple immune regulatory mechanisms and cell types are likely at play to assure successful pregnancy. Therefore, it is important to understand the complete microenvironment of the decidua, preferably in the context of the whole immune cell repertoire of the pregnant woman. So far, most studies have focused on a single mechanism or cell type, which often is the FoxP3 positive regulatory T cell when studying immune regulation. In this review, we instead focus on the contribution of FoxP3 negative Treg subsets to the decidual microenvironment and their possible role in pregnancy complications. Their phenotype, function, and effect in pregnancy are discussed.

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Expression of TGF-β1 and miR-99a in serum of patients with early spontaneous abortion and correlation with hormone levels during pregnancy

Cited by 7 publications

References 19 publications

MicroRNA-99a is a Potential Target for Regulating Hypothalamic Synaptic Plasticity in the Peri/Postmenopausal Depression Model

MicroRNA-99a is a Potential Target for Regulating Hypothalamic Synaptic Plasticity in the Peri/Postmenopausal Depression Model

Dysregulation of lncRNA SNHG1/miR‑145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis

Regulatory T Cells in Pregnancy: It Is Not All About FoxP3

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