scholarly journals Role of Antioxidant Vitamins in Neurogenesis

2021 ◽  
Vol 15 (1) ◽  
pp. 11
Author(s):  
Shreyashish Roy-Chowdhury ◽  
Daivat Bhavsar ◽  
Jasrita Singh ◽  
Austin Mardon
Keyword(s):  
Cell Proliferation ◽  
Neural Differentiation ◽  
Scientific Evidence ◽  
Antioxidant Vitamins ◽  
Antioxidant Vitamin ◽  
Regulatory Factor ◽  
Functional Aspects ◽  
Cycle Regulation ◽  
Inhibit Cell Proliferation

Neurogenesis is vital in the preservation of cognition. Previous studies have reported antioxidant vitamins as a key regulatory factor in neurogenesis. However, current research investigating their role is inconclusive due to the limited number of studies that have been conducted and conflicting results. This review evaluates the scientific evidence behind the potential roles of antioxidant vitamins in neurogenesis. Observations concerned with the mechanistic and functional aspects of how antioxidant vitamins modulate neurogenesis are both assessed. Vitamin A is evidently involved in cell cycle regulation and cell proliferation; vitamin C reportedly promotes neural differentiation and maturation while inhibiting neurite outgrowth; vitamin E is identified to inhibit cell proliferation while improving cell viability. Varying antioxidant vitamin concentrations have been implicated in facilitating cognition in terms of attention, memory, language, and executive function. Moreover, this review suggests a threshold antioxidant vitamin concentration that should be maintained to promote optimal levels of adult neurogenesis.

scholarly journals Knock-Down of the NFAT2 Long and Intermediate Isoforms Leads to CLL Acceleration

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4371-4371
Author(s):  
Jonas S Heitmann ◽  
Melanie Märklin ◽  
Posdorowkin Anastasia ◽  
Alexander R Fuchs ◽  
Felicia M Truckenmüller ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
B Cells ◽  
Conflicts Of Interest ◽  
Cell Types ◽  
Knock Down ◽  
Nsg Mice ◽  
Selective Ablation ◽  
Cycle Regulation

Abstract NFAT2 is a highly phosphorylated transcription factor which regulates developmental and activation programs in diverse cell types. We and others have previously described a significant overexpression of NFAT2 in CLL cells as compared to physiological B cells. Three major isoforms of NFAT2 with different regulatory properties have been described (700aa short isoform, 800aa intermediate isoform, 900 aa long isoform). Here, we analyzed the role of different NFAT2 transcripts in CLL with respect to disease phenotype and cell proliferation. We investigated primary samples from CLL patients (n=30) for their expression profile of different NFAT2 isoforms using RT-PCR. Applying an shRNA approach, we generated stable knock-down cells of the CLL cell line MEC-1 for the long and intermediate isoforms and for the entire NFAT2 gene resulting in the complete ablation of all isoforms. The proliferation properties of the different MEC-1 cell lines was subsequently assessed in xeno-transplant experiments into NSG mice. While physiological B cells express comparable levels of the short and intermediate/long isoforms, we could detect a five fold overexpression of the intermediate/long isoforms in primary CLL samples. To further analyze the differential regulation of the different NFAT2 transcripts on tumor cell proliferation and cell cycle regulation, we injected NSG mice with MEC-1 cells with intact NFAT2 (n=6), MEC-1 cells with a knock-down of the intermediate and long isoforms (n=6) and MEC-1 cells with a complete NFAT2 knock-down (n=6). MEC-1 cells with selective ablation of the intermediate and long NFAT2 isoforms grew significantly faster in NSG mice than MEC-1 cells with intact NFAT2 expression or MEC-1 cells with a complete NFAT2 knock-down. MEC-1 cells selectively lacking the intermediate and long isoforms led to accelerated tumor proliferation upon subcutaneous injection. Cell cycle analysis as assessed by flow cytometry showed a significantly increased number of cells in the G1/S-Phase for the group without expression of the short isoform, while the group with complete NFAT knock-down exhibited a compromised growth pattern as compared to wild-type MEC-1 cells. In summary, our data demonstrate that genetic loss of the intermediate and long isoforms of NFAT2 leads to CLL acceleration Disclosures No relevant conflicts of interest to declare.

Inhibition of cell proliferation and induction of apoptosis by N1,N11-diethylnorspermine-induced polyamine pool reduction

2007 ◽  
Vol 35 (2) ◽  
pp. 405-409 ◽  
Author(s):  
S.M. Oredsson ◽  
K. Alm ◽  
E. Dahlberg ◽  
C.M. Holst ◽  
V.M. Johansson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Regulation ◽  
Meta Analysis ◽  
Short Review ◽  
Cell Cycle Kinetics ◽  
Polyamine Analogue ◽  
Induction Of Apoptosis ◽  
Cycle Regulation

Reduction of cellular polyamine pools results in inhibition of cell proliferation and sometimes in induction of cell death. Reduction of cellular polyamine pools can be achieved by several strategies involving all the mechanisms of polyamine homoeostasis, i.e. biosynthesis, catabolism and transport across the cell membrane. In the present paper, we concentrate on results achieved using the polyamine analogue DENSPM (N1,N11-diethylnorspermine) on different cell lines. We discuss polyamine levels in DENSPM-treated cells in relation to effects on cell cycle kinetics and induction of apoptosis. To really understand the role of polyamines in cell cycle regulation and apoptosis, we believe it is now time to go through the vast polyamine literature in a meta-analysis-based manner. This short review does not claim to be such a study, but it is our hope to stimulate such studies in the polyamine field. Such work is especially important from the viewpoint of introducing drugs that affect polyamine homoeostasis in the treatment of various diseases such as cancer.

The Role of Zinc in Thyroid Hormones Metabolism

2019 ◽  
Vol 89 (1-2) ◽  
pp. 80-88 ◽  
Author(s):  
Juliana Soares Severo ◽  
Jennifer Beatriz Silva Morais ◽  
Taynáh Emannuelle Coelho de Freitas ◽  
Ana Letícia Pereira Andrade ◽  
Mayara Monte Feitosa ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Scientific Evidence ◽  
Thyroid Stimulating Hormone ◽  
Zinc Transporters ◽  
Serum Concentrations ◽  
Metabolic Adaptations ◽  
Serum T3 ◽  
Regulatory Effects ◽  
Shed Light

Abstract. Thyroid hormones play an important role in body homeostasis by facilitating metabolism of lipids and glucose, regulating metabolic adaptations, responding to changes in energy intake, and controlling thermogenesis. Proper metabolism and action of these hormones requires the participation of various nutrients. Among them is zinc, whose interaction with thyroid hormones is complex. It is known to regulate both the synthesis and mechanism of action of these hormones. In the present review, we aim to shed light on the regulatory effects of zinc on thyroid hormones. Scientific evidence shows that zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating deiodinases enzymes activity, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) synthesis, as well as by modulating the structures of essential transcription factors involved in the synthesis of thyroid hormones. Serum concentrations of zinc also appear to influence the levels of serum T3, T4 and TSH. In addition, studies have shown that Zinc transporters (ZnTs) are present in the hypothalamus, pituitary and thyroid, but their functions remain unknown. Therefore, it is important to further investigate the roles of zinc in regulation of thyroid hormones metabolism, and their importance in the treatment of several diseases associated with thyroid gland dysfunction.

Adhesion barriers inhibit cell proliferation, adhesion and invasion of primary endometriosis cells

2014 ◽  
Vol 74 (S 01) ◽  
Author(s):  
SP Renner ◽  
MW Beckmann ◽  
S Burghaus ◽  
R Strick ◽  
PL Strissel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Adhesion And Invasion ◽  
Inhibit Cell Proliferation

TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Lymphatic Invasion ◽  
Cancer Specific Survival ◽  
Candidate Target ◽  
Candidate Target Gene ◽  
And Migration

TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression andits function in renal cell carcinoma (RCC) are still unknown. Here in this study, weinvestigated the clinical significance of TRIM44 and its biological function in RCC.TRIM44 overexpression was significantly associated with clinical M stage, histologictype (clear cell) and presence of lymphatic invasion (P = .047, P = .005, and P = .028,respectively). Moreover, TRIM44 overexpression was significantly associated withpoor prognosis in terms of cancer-specific survival (P = .019). Gain-of-function andloss-of-function studies using TRIM44 and siTRIM44 transfection showed thatTRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1and 769P. To further investigate the role of TRIM44 in RCC, we performed integratedmicroarray analysis in Caki1 and 769P cells and explored the data in the Oncominedatabase. Interestingly, FRK was identified as a promising candidate target gene ofTRIM44, which was downregulated in RCC compared with normal renal tissues. Wefound that cell proliferation was inhibited by TRIM44 knockdown and then recoveredby siFRK treatment. Taken together, the present study revealed the associationbetween high expression of TRIM44 and poor prognosis in

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