Effects of female sex hormones on folic acid–induced anti‐angiogenesis

Lee, W.-S.; Lu, Yichen; Kuo, Chun-Ting; Chen, C.-T.; Pl, Tang

doi:10.1111/apha.13001

Cited by 6 publications

(4 citation statements)

References 34 publications

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“…Since angiogenesis is critical for placental function and development, we verified expression changes of several genes involved in angiogenesis, including 18 genes in the HIF pathway, VEGF pathway, S1P signaling, extracellular matrix formation, or other functions known to affect vascular health. Some studies have reported the impact of folate on angiogenesis, [13,14] but these studies were largely in vitro whereas our work examined folate intake in vivo. Furthermore, the impact of folate on expression of the afore-mentioned genes in angiogenesis has not been reported.…”

Section: Discussionmentioning

confidence: 99%

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Moderate Folic Acid Supplementation in Pregnant Mice Results in Altered Methyl Metabolism and in Sex‐Specific Placental Transcription Changes

Liang

Leclerc

Cosín-Tomás

et al. 2021

Molecular Nutrition Food Res

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Scope: Many pregnant women have higher folic acid (FA) intake due to food fortification and increased vitamin use. It is reported that diets containing five-fold higher FA than recommended for mice (5xFASD) during pregnancy resulted in methylenetetrahydrofolate reductase (MTHFR) deficiency and altered choline/methyl metabolism, with neurobehavioral abnormalities in newborns. The goal is to determine whether these changes have their origins in the placenta during embryonic development. Methods and Results: Female mice are fed control diet or 5xFASD for a month before mating and maintained on these diets until embryonic day 17.5. 5xFASD led to pseudo-MTHFR deficiency in maternal liver and altered choline/methyl metabolites in maternal plasma (increased methyltetrahydrofolate and decreased betaine). Methylation potential (S-adenosylmethionine:S-adenosylhomocysteine ratio) and glycerophosphocholine are decreased in placenta and embryonic liver. Folic acid supplemented diet results in sex-specific transcriptome profiles in placenta, with validation of dietary expression changes of 29 genes involved in angiogenesis, receptor biology or neurodevelopment, and altered methylation of the serotonin receptor 2A gene. Conclusion: Moderate increases in folate intake during pregnancy result in placental metabolic and gene expression changes, particularly in angiogenesis, which may contribute to abnormal behavior in pups. These results are relevant for determining a safe upper limit for folate intake during pregnancy.

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Section: Discussionmentioning

confidence: 99%

“…[11] FA can promote angiogenesis, [12] although some studies have suggested an anti-angiogenesis role. [13,14] Placenta can affect fetal organ development, including brain. Many neurobehavioral disorders trace their origin to placenta.…”

Section: Introductionmentioning

confidence: 99%

Moderate Folic Acid Supplementation in Pregnant Mice Results in Altered Methyl Metabolism and in Sex‐Specific Placental Transcription Changes

Liang

Leclerc

Cosín-Tomás

et al. 2021

Molecular Nutrition Food Res

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“…Another female sex‐specific effect has recently been described by Lee et al, who report an antiangiogenic effect of folate, which seems to be counteracted by pregnancy‐related female hormones . Further research is needed to, in detail, observe and interpret potential related effects in human subjects.…”

mentioning

confidence: 88%

Foetal programming

Persson

2019

Acta Physiologica

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“…Upon binding to the VEGF receptor 2 (VEGFR2) on ECs, VEGF activates quiescent ECs and initiates angiogenesis, ensuring the reestablishment of oxygen and nutrients in the tissue [36,37]. However, other bioactive molecules, including growth factors [38], cytokines [39,40], hormones [41], and non-coding RNAs, such as microRNAs (miRNA) and long non-coding RNAs (lncRNA), also regulate angiogenesis [42].…”

Section: Endothelial Function Is Versatilementioning

confidence: 99%

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Kulovic-Sissawo,

Tocantins,

Diniz

et al. 2024

Biology

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Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.

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Effects of female sex hormones on folic acid–induced anti‐angiogenesis

Abstract: Female sex hormones interrupt the FA-induced anti-angiogenic action through receptor-receptor interaction.

Cited by 6 publications

References 34 publications

Moderate Folic Acid Supplementation in Pregnant Mice Results in Altered Methyl Metabolism and in Sex‐Specific Placental Transcription Changes

Moderate Folic Acid Supplementation in Pregnant Mice Results in Altered Methyl Metabolism and in Sex‐Specific Placental Transcription Changes

Foetal programming

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

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