China
Africa
Explore chapters and articles related to this topic
Vitexin: Phytochemical and Pharmacological Significance
Published in V. R. Mohan, A. Doss, P. S. Tresina, Ethnomedicinal Plants with Therapeutic Properties, 2019
Vitexin 2″-O-rhamnoside and vitexin 4″-O-glucoside are the two main flavonoid glycosides of the leaves of C. pinnatifida Bge. var. major N.E.Br. that has been widely used for the treatment of cardiovascular system diseases (Wei et al., 2014). Vitexin has the potential to protect against cardiac hypertrophy through Ca2+-mediated calcineurin-NFATc3 and CaMKII signaling pathways (Lu et al., 2013). It has a protective effect against myocardial ischemia-reperfusion (I/R) injury in rat heart in vivo, which may be associated with the antioxidation and inhibition of the release of inflammatory cytokines via attenuating expression of NF-χBp65 and TNF-α, as well as the upregulation of phospho-ERK and the downregulation of phospho-c-Jun expression (Dong et al., 2013).
A comprehensive analysis of Wnt/β-catenin signaling pathway-related genes and crosstalk pathways in the treatment of As2O3 in renal cancer
Published in Renal Failure, 2018
Yan-Lei Li, Yu-Fen Jin, Xiu-Xia Liu, Hong-Jun Li
NFATC3 encodes a member of the nuclear factors of activated T cells DNA-binding transcription complex, and it is important for T-cell development and essential for cancer chemoresistance [34]. NFAT proteins are able to inhibit the Wnt/β-catenin pathway via participating in regulating cell proliferation and differentiation [35,36]. Study has reported that NFAT signaling controls nephron formation, and NFATC3 is abundantly expressed in the metanephric mesenchyme [37]. In de novo renal allograft recipients, expression levels of NFAT-regulated genes are closely related to the clinical outcomes [38]. Furthermore, NFAT has been recently demonstrated to play pivotal roles in kidney ischemia/reperfusion (I/R) injury [39]. There is no evidence to support the association of NFATC3 with renal cancer so far, while the increased NFATC3 expression has been detected in human angiosarcoma that was induced by secreted frizzle-related protein 2 (SFRP2) [40]. Collectively, As2O3 treatment may affect the Wnt/β-catenin pathway through decreasing the expression of NFATC3 in renal cancer.
Correlation of the transcription factors IRF4 and BACH2 with the abnormal NFATC1 expression in T cells from chronic myeloid leukemia patients
Published in Hematology, 2022
Yikai Zhang, Xiangbo Zeng, Xianfeng Zha, Jing Lai, Guangxiao Tan, Shaohua Chen, Xibao Yu, Yangqiu Li, Ling Xu
To determine potential reasons for NFATC1 down-regulation in T cells from CML patients. We compared the results which predicted by hTFtarget database with the DEGs identified by microarray analysis. As shown in Figure 3(A,B), there were 24 potential transcriptional regulators of NFATC1 that were altered. We next analyzed the correlation between the 24 transcription factors and NFATC1 (Figure S1). The results demonstrated that 21 transcription factors correlated with NFATC1, including eight genes that were positively correlated and thirteen genes that were negatively correlated. It has been reported that BTB domain and CNC homolog 2 (BACH2) [32–34] and interferon regulating factor 4 (IRF4) [35,36] are involved in regulating T cell function. It has been reported that NFAT family members NFATC1, NFATC2, and NFATC3 are also expressed in T cells and participate in the regulation of T cell function [37–40]. Thus, we examined the expression level of BACH2, IRF4, NFATC1, NFATC2, and NFATC3 in the CD3+ T cells from CML patients and healthy donors. As shown in Figure 3(C), the expression of BACH2 (p < 0.01), IRF4 (p < 0.01), NFATC1 (p < 0.01), and NFATC3 (p < 0.001) in CML patient T cells was significantly lower than that in healthy donors. We further analyzed the correlation between these genes and NFATC1, and the results demonstrated that the expression of IRF4 (R = 0.538, p = 0.047), BACH2 (R = 0.697, p = 0.006) and NFATC3 (R = 0.875, p < 0.001) were positively correlated with NFATC1 (Figure 3(D)). The PPI analysis also shown that there was an interaction between NFATC1 and IRF4, while BACH2 shown an interaction with IRF4 (Figure 3(E)).
Oral administration of green tea Epigallocatechin-3-gallate reduces oxidative stress and enhances restoration of cardiac function in diabetic rats receiving autologous transplantation of adipose-derived stem cells
Published in Archives of Physiology and Biochemistry, 2021
Tung-Sheng Chen, Show-Yih Liou, Hsin-Hung Lin, Meng-Yu Hung, Chien-Chung Lin, Yueh-Min Lin, Kuan-Ho Lin, V. Vijaya Padma, Chun-Hsu Yao, Wei-Wen Kuo, Chih-Yang Huang
Elevation of ROS induced by DM not only activates pro-apoptotic signalings, but also triggers pathological signalings including cardiac inflammation, hypertrophy, and fibrosis (Ko et al. 2013, Zhong et al. 2015, Zheng et al. 2015). In cardiomyocytes, inflammatory responses can be activated by ROS through toll-like receptor 4/nuclear factor-κB (TLR4/NFκB) pathway under high glucose environment. Activation of TLR4/NFκB axis lead to express of inflammatory proteins, including cyclooxygenase 2 (Cox 2) and cytokines. Then the expression of inflammatory mediators also activates inflammatory responses through autocrine or paracrine, resulting in amplifying inflammation in cardiomyocytes under high glucose environment (Zhong et al. 2015). Previous studies mention that ROS also induces imbalance of calcium flux in cardiomyocytes. Imbalance of calcium flux then activates a protein called calcineurin. The calcineurin is a phosphatase. In cardiomyocytes, calcineurin can induce dephosphorylation of nuclear factor of activated T-cells 3 (NFATc3), and dephosphorylated NFATc3 then translocates to nucleus. Nuclear translocation of NFATc3 induces transcription and translation of hypertrophy proteins such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and myosin heavy chain beta (MHC-β), leading to cardiac hypertrophy (Liu et al. 2015). In addition to inflammatory and hypertrophy responses, cardiac fibrosis induced by ROS also can be observed in cardiomyocytes under high glucose environment. In vivo studies provide evidence to indicate that transforming growth factor beta (TGF β) is highly expressed in animal hearts with DM. Expression of TGFβ then activates small mothers against decapentaplegic (smad) proteins (except smad6/7) to translocate to nucleus, leading to encode fibrotic proteins including collagen and matrix metalloproteinases (MMPs) (Liu et al. 2013, Bugyei-Twum et al. 2014).