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- Bajbouj, Khuloud, et al.
(författare)
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Elevated Levels of Estrogen Suppress Hepcidin Synthesis and Enhance Serum Iron Availability in Premenopausal Women
- 2018
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Ingår i: Experimental and clinical endocrinology & diabetes. - : Georg Thieme Verlag KG. - 0947-7349 .- 1439-3646. ; 126:07, s. 453-459
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Tidskriftsartikel (refereegranskat)abstract
- Clinical and experimental observations have long suggested that elevated levels of estrogen associate with increased serum iron availability. Additionally, recent work has shown that estrogen can downregulate hepcidin synthesis in vitro. This study aims at assessing whether the ability of estrogen to downregulate hepcidin synthesis translates into changes in serum iron status. Hepcidin synthesis was evaluated in MCF-7, Hep-G2 and SKOV-3 cells treated with increasing concentrations of estrogen and cultured for up to 24 h post treatment. The correlation between levels of serum estrogen, hepcidin and iron was assessed using serum samples collected from 153 premenopausal women at random and samples collected from 6 women at days 1, 5, 10, 16, 21 and 28 of the monthly cycle. Estrogen-treated MCF-7 cells showed a significant reduction in hepcidin synthesis, especially at 20 nM/24 h E2 treatment. Hepcidin synthesis was also significantly reduced in Hep-G2 and SKOV-3 cells at 20 nM/24 h E2 treatment. In serum samples collected at random, estrogen (P=0.022; R=-0.213) and iron (P=0.028; R=-0.316) correlated negatively with hepcidin and positively with each other (P=0.033; R=0.319). An overall similar pattern was also observed in monthly cycle-timed samples. These findings suggest that elevated levels of estrogen reduce hepcidin synthesis as means of enhancing serum iron content in menstruating women.
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| 2. |
- Madkour, Mohamed I., et al.
(författare)
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Ramadan diurnal intermittent fasting modulates SOD2, TFAM, Nrf2, and sirtuins (SIRT1, SIRT3) gene expressions in subjects with overweight and obesity
- 2019
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Ingår i: Diabetes Research and Clinical Practice. - Shannon, Ireland : Elsevier Ireland Ltd.. - 0168-8227 .- 1872-8227. ; 155
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Tidskriftsartikel (refereegranskat)abstract
- Aim: A growing body of evidence supports the impact of intermittent fasting on normalizing body metabolism and lowering oxidative stress and inflammation. Mounting evidence confirms that oxidative stress and chronic inflammation trigger the way for the development of metabolic diseases, such as diabetes. This research was conducted to evaluate the impact of Ramadan intermittent fasting (RIF) on the expression of cellular metabolism (SIRT1 and SIRT3) and antioxidant genes (TFAM, SOD2, and Nrf2).Methods: Fifty-six (34 males and 22 females) overweight and obese subjects and six healthy body weight controls were recruited and monitored before and after Ramadan.Results: Results showed that the relative gene expressions in obese subjects in comparison to counterpart expressions of controls for the antioxidant genes (TFAM, SOD2, and Nrf2) were significantly increased at the end of Ramadan, with percent increments of 90.5%, 54.1% and 411.5% for the three genes, respectively. However, the metabolism-controlling gene (SIRT3) showed a highly significant (P < 0.001) downregulation accompanied with a trend for reduction in SIRT1 gene at the end of Ramadan month, with percent decrements of 61.8% and 10.4%, respectively. Binary regression analysis revealed significant positive correlation (P < 0.05) between high energy intake (>2000 Kcal/day vs. <2000 Kcal/day) and expressions of SOD2 and TFAM (r = 0.84 and r = 0.9, respectively).Conclusion: Results suggest that RIF ameliorates the genetic expression of antioxidant and anti-inflammatory, and metabolic regulatory genes. Thus, RIF presumably may entail a protective impact against oxidative stress and its adverse metabolic-related derangements in non-diabetic obese patients.
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| 3. |
- Omar, Hany A., et al.
(författare)
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Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment
- 2019
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Ingår i: The FEBS Journal. - : John Wiley & Sons. - 1742-464X .- 1742-4658. ; 286:18, s. 3540-3557
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Forskningsöversikt (refereegranskat)abstract
- Cancer immunotherapy represents a promising new era in cancer management due to the relatively high safety margins and selectivity, compared to the classical cancer chemotherapeutic agents. However, there is an imperative need to overcome tumor resistance in order to improve clinical outcomes and maximize the benefits of cancer immunotherapy. The interaction between the programmed cell death-1 (PD-1) receptor and its ligand PD-L1 is a vital immune checkpoint that is often adopted by cancer cells to undergo immune evasion. PD-1/PD-L1 signaling is regulated at multiple levels through the crosstalk with other immune targets or relevant signaling partners involved in the cancer progression. Among the significant epigenetic players that are implicated in modulating the immune system are microRNAs (miRNAs). A complex system of these noncoding RNAs regulates the gene expression at the post-transcriptional level and plays a significant role in the modulation of both innate and the adaptive immune systems. The expression profile of immune-modulatory miRNAs might be useful as a predictive biomarker for the response and clinical outcomes in cancer immunotherapy. Therefore, in the current review, we highlighted the role of miRNAs in cancer immune evasion through a critical discussion of their impact on key immune checkpoints as well as the role of miRNAs in cancer progression and resistance.
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