miRNA as a New Regulatory Mechanism of Estrogen Vascular Action

Pérez‐Cremades, Daniel; Mompeón, Ana; Vidal‐Gómez, Xavier; Hermenegildo, Carlos; Novella, Susana

doi:10.3390/ijms19020473

Cited by 38 publications

(30 citation statements)

References 123 publications

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“…Through bioinformatics analysis, we found a regulatory relationship between the differentially expressed genes and microRNAs after E2 treatment. miRNA has been widely reported to be involved in E2 regulation (20)(21)(22). Through miRNA-target gene prediction, we found miR-148a and miR-152 have binding sequences on the 3'UTR of ADCY2 (Fig.…”

Section: E2 Promotes Adcy2 Expression Through Inhibiting Mir-148a/mirmentioning

confidence: 91%

Estrogen Promotes cAMP Production in Mesenchymal Stem Cells by Regulating ADCY2

Zhao

Miao

et al. 2020

IJSC

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Background and Objectives: The maternal-fetal interface is an important source of mesenchymal stem cells (MSCs), and it is influenced by high levels of estradiol (E2) during pregnancy. It is highly important to study the role of E2 in MSCs for both clinical application and understanding of the mechanisms underlying pregnancy related diseases. Methods and Results: In this study, differently expressed genes (DEGs) were found in the MSCs after exposure to E2. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs was performed and the integrated regulatory network of DEGs-miRNA was constructed. A total of 390 DEGs were found in the MSCs exposed to E2, including 164 upregulated DEGs (e.g. ADCY2, VEGFA and PPY) and 226 downregulated DEGs (e.g. KNG1, AGT and NPY). Additionally, 10 miRNAs (such as miR-148A/B, miR-152, miR-182) identified the integrated regulatory network of DEGs-miRNAs. Among them, the expression of ADCY2 was significantly upregulated, and this was associated with multiple changed genes. We confirmed that the expression of ADCY2 is significantly promoted by E2 and subsequently promoted the production of cAMP in MSCs. We also found that E2 promoted ADCY2 expression by inhibiting miR-152 and miR-148a. Conclusions: E2 promotes the expression of cAMP through miR-148a/152-ADCY2 in MSCs. It is suggested that E2 plays a key role in the growth and function of MSCs.

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Section: E2 Promotes Adcy2 Expression Through Inhibiting Mir-148a/mirmentioning

confidence: 91%

Estrogen Promotes cAMP Production in Mesenchymal Stem Cells by Regulating ADCY2

Zhao

Miao

et al. 2020

IJSC

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“…A recent study showed that 17 b-estradiol attenuates angiotensin IIeinduced H3 acetylation in the aorta and investigations proving the involvement of microRNAs in estrogen-related vascular biology support the probability of epigenetic changes playing a role. [42][43][44] Moreover, because shorter RLDs are linked with longer durations of estrogen deficiency, the findings of the study may suggest a harmful effect of estrogen deficiency rather than a protective role of estrogen. Further evaluations would be needed to elucidate clearly whether these possibilities have significant biomolecular applications.…”

Section: Discussionmentioning

confidence: 87%

Association of Reproductive Lifespan Duration and Chronic Kidney Disease in Postmenopausal Women

Kang

Jhee

Joo

et al. 2020

Mayo Clinic Proceedings

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Objective: To investigate the relationship between endogenous estrogen exposure and renal function, the association of female reproductive life span duration (RLD) and chronic kidney disease (CKD) was analyzed in postmenopausal women. Patients and Methods: Data were retrieved from the Korean Genome and Epidemiology Study, which was constructed from May 1, 2001, through December 25, 2017. A total of 50,338 and 3155 postmenopausal women were each included in the cross-sectional and longitudinal analyses. The RLD was determined by subtracting the age at menarche from the age at menopause. Participants were grouped into RLD quartiles. Participants with estimated glomerular filtration rates less than 60 mL/min/1.73 m 2 were regarded to have CKD. Results: In the cross-sectional analysis, mean AE SD age and estimated glomerular filtration rate were 56.3AE4.9 years and 93.1AE13.6 mL/min/1.73 m 2 , respectively. Mean AE SD RLD was 34.2AE4.0 years. A total of 765 of 50,338 (1.52%) women were found to have CKD. Logistic regression analysis revealed that the odds ratio for CKD was lower in groups with longer RLDs as compared with the shortest RLD group. In longitudinal analysis, postmenopausal women with normal kidney function were followed up for 9.7 years and incident CKD occurred in 221 of 3155 (7.00%) participants. Cox analysis revealed that the risk for CKD development was significantly lower in longer RLD groups. This finding was significant even after adjustments for confounding factors. Conclusion: The risk for CKD was lower in women with longer RLDs. The amount of endogenous estrogen exposure could be a determining factor for renal function in postmenopausal women.

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“…), transcriptomic data in human endothelial cells treated with physiological concentrations of oestradiol highlight the changes in the expression of specific genes involved in miRNA synthesis (Pérez‐Cremades et al . ).…”

Section: Oestrogen Receptors In the Cardiovascular Systemmentioning

confidence: 97%

Mechanisms underlying the influence of oestrogen on cardiovascular physiology in women

Novella

Pérez‐Cremades

Mompeón

et al. 2019

The Journal of Physiology

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Women show a lower incidence of cardiovascular diseases than age‐matched men, but this benefit disappears after menopause. Oestrogen‐mediated vascular actions are mainly attributed to oestradiol and exerted by oestrogen receptors (ERα, ERβ and G protein‐coupled oestrogen receptor), through rapid and/or genomic mechanisms, but these effects depend on ageing and inflammation. A cardiovascular approach in women's health has arisen due to controversy regarding oestrogen's beneficial impact as reported in experimental and observational studies and large randomized trials. These can be explained, in part, by two mutually non‐exclusive hypotheses. On the one hand, the timing hypothesis, which states that oestrogen‐mediated benefits occur before the detrimental effects of ageing are established in the vasculature; on the other hand, ageing and/or hormonal‐associated changes in ER expression that could lead to a deleterious imbalance in favour of ERβ over ERα, generally associated with higher inflammation and endothelial dysfunction. In experimental studies, oestradiol acting on ERα promotes the release of vasoactive compounds such as nitric oxide (NO) and prostacyclin, and shifts the angiotensin axis towards angiotensin 1–7 production. Mechanisms underlying oestradiol vascular function also include anti‐inflammatory and epigenetic modifications. 17β‐Oestradiol changes the transcriptomic profile of endothelial cells, and the involvement of miRNA in the regulatory pathways of vascular function reinforces assumptions regarding the vascular actions of oestrogen. Thus, the present Symposium Review aims to postulate the role of ERα in oestrogen modulation of endothelium‐derived mediators and vascular physiology, as well as its relationship with miRNA and inflammation, and elucidate how physiological changes in postmenopausal women counteract the observed effects.

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miRNA as a New Regulatory Mechanism of Estrogen Vascular Action

Cited by 38 publications

References 123 publications

Estrogen Promotes cAMP Production in Mesenchymal Stem Cells by Regulating ADCY2

Estrogen Promotes cAMP Production in Mesenchymal Stem Cells by Regulating ADCY2

Association of Reproductive Lifespan Duration and Chronic Kidney Disease in Postmenopausal Women

Mechanisms underlying the influence of oestrogen on cardiovascular physiology in women

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