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MOF-based Electrochemical Sensors for DNA/RNA/ATP
Published in Ram K. Gupta, Tahir Rasheed, Tuan Anh Nguyen, Muhammad Bilal, Metal-Organic Frameworks-Based Hybrid Materials for Environmental Sensing and Monitoring, 2022
Saadat Majeed, Muhammad Umer Farooq, Sayed Tayyab Raza Naqvi, Batool Fatima, Muhammad Najam-ul-Haq, Sabahat Majeed, Fahad Ali, Naeem Akhtar Khan
miRNA-122 is a biomarker of drug-induced liver injury. An electrochemical biosensor for this marker was developed by a team of researchers. A nanocomposite material of Fe-MIL-88- NH2, Streptavidin, hairpin signal probe (H2), and palladium nanoparticles were synthesized due to its good catalytic properties which act as a signal unit. While glassy carbon electrodes (GCE) The GCE was modified with nitrogen-doped graphene sheets and a heparin capture probe (H1). Upon addition of miRNA-122, H1 present at the surface of the GCE will open up and become hybridized with miRNA. The addition of MOF-based material leads to the release of miRNA-122 from H1 and the formation of a new stable H1-H2 hybrid takes place. In this assay, sensitivity and the linear range were recorded up to 0.003 fM and 0.01 to 10 pM, respectively. This study was applied on spiked serum samples as well as blood with excellent recovery and selectivity [39].
MicroRNAs
Published in Peixuan Guo, Kirill A. Afonin, RNA Nanotechnology and Therapeutics, 2022
Bin Guo, Jingwen Liu, Daniel W. Binzel
miRNAs play a critical role in the cardiovascular system. They are involved in myocardial infarction (Bonauer et al., 2009, van Rooij et al., 2008), cardiac hypertrophy (Care et al., 2007), cardiac fibrosis (Zhao et al., 2015), arrhythmia (Cheng et al., 2019), vascular diseases (Hartmann et al., 2016), and heart failure (Thum et al., 2007). In the first experiment that demonstrates the efficacy of cholesterol-conjugated antagomiRs in mouse, Krutzfeldt et al. successfully inhibited miR-122 in the liver, resulting in the downregulation of cholesterol biosynthesis genes and a reduction of the plasma cholesterol level (Krutzfeldt et al., 2005). In a breakthrough study, Rayner et al. successfully increased plasma high-density lipoprotein (HDL) levels and reduced plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides in African green monkeys, using systemic delivery of an antagomiR that targets both miR-33a and miR-33b (Rayner et al., 2011). Using a cholesterol-conjugated antagomiR inhibitor of miR-133, Care et al. demonstrated that a single infusion of the antagomiR can cause marked and sustained cardiac hypertrophy (Care et al., 2007). MiR-21 expression increases in fibroblasts of the failing heart, and Thum et al. found that silencing of miR-21 with an antagomiR inhibits interstitial fibrosis and attenuates cardiac dysfunction (Thum et al., 2008). MiRNAs also regulate the functions of endothelial cells. For example, Fiedler et al. showed that miR-24 is upregulated in cardiac endothelial cells and induces apoptosis after cardiac ischemia (Fiedler et al., 2011). Inhibition of miR-24 with cholesterol-conjugated antagomiR reduced the size of myocardial infarction in mice, prevented endothelial apoptosis, enhanced vascularity, and preserved cardiac function and survival (Fiedler et al., 2011). MiRNAs can directly regulate cardiomyocyte survival. Overexpression of miR-320 enhanced cardiomyocyte death and apoptosis and a single tail vein injection of cholesterol-modified antagomiR of miR-320 prevented apoptosis and reduced infarction size in mice (Ren et al., 2009b). In atrial fibrillation patients, miR-320 expression is increased in the atria and suppresses the cardiac L-type Ca2+ channel. Blocking miR-328 with an antagomiR reversed atrial fibrillation, and genetic knockdown of endogenous miR-328 reduced the vulnerability to atrial fibrillation in mice (Lu et al., 2010).
MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver
Published in International Journal of Environmental Health Research, 2022
Rui Wang, Haohao Liu, Xingde Du, Ya Ma, Zhihui Tian, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang
MC-LR is a potential carcinogen for animals and humans. The International Agency for Research on Cancer (IARC) has listed MC-LR as a suspected human carcinogen (category 2B) Liu et al. (2021). Clinically, miR-122 is an important tumor suppressor, and its liver and circulating levels are prognostic indicators for patients with liver cancer Xu et al. (2011). In animal models, the specific expression of hepatocytes and their release from damaged hepatocytes early in liver injury make miR-122 an attractive biomarker for liver injury. It plays an important role in maintaining the phenotype of the liver, and its loss of function can induce the hepatocarcinogenesis Hsu et al. (2012). The previous research of our group has shown that after C57BL/6 mice are exposed to MC-LR for two weeks, miR-122 gene expression was reduced by more than 70% Wang et al. (2020). Then, the role and mechanism of miR-122 in the process of hepatocarcinogenesis induced by MC-LR need further exploration.