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Genetics and Genetic Testing in Hypertrophic Cardiomyopathy
Published in Srilakshmi M. Adhyapak, V. Rao Parachuri, Hypertrophic Cardiomyopathy, 2020
Multi-gene panels are commonly used for HCM genetic testing. Different laboratories, commercial or research based, will have variations in the composition of their gene panels. But, generally, the panels will often include a wide array of sarcomere genes, which have a proven genetic basis with the phenotypic expression of HCM. An HCM genetic panel will usually include well-described sarcomere genes such as myosin-binding protein C (MYBPC3), the myosin heavy chain (MYH7), cardiac troponin T(TNNT2), cardiac troponin I (TNNI3), alpha-tropomyosin (TPM1), myosin essential and regulatory light chains (MYL2, MYL3), and cardiac actin (ACTC) [8].
Assessing the clinical utility of multi-omics data for predicting serous ovarian cancer prognosis
Published in Journal of Obstetrics and Gynaecology, 2023
Zhe Zhang, Zhiyao Wei, Luyang Zhao, Chenglei Gu, Yuanguang Meng
First, we performed an intersection analysis between different types of molecular features. Interestingly, for the therapeutic model, we found that the mRNA expression of genes and the DNA methylation levels of gene promoters overlapped significantly (p = .00807). Among the overlapped gene signatures of the survival model, POLD2 and MYL2 were present in three groups at the same time. These two genes were previously identified by other studies as biomarkers predicting the survival of OC patients. Additionally, we found that CXCL9, CACNA2D1 and EHD1 were notable markers associated with patient survival. Among the overlapped gene signatures of the therapeutic models, GABARBP, CXCL11, JAG1, FANCA, and CABIN1 were associated with chemotherapies administered to HGSOC patients.
Different cellular mechanisms from low- and high-dose zinc oxide nanoparticles-induced heart tube malformation during embryogenesis
Published in Nanotoxicology, 2022
Mengwei Wang, Ping Zhang, Zeyu Li, Yu Yan, Xin Cheng, Guang Wang, Xuesong Yang
Using bioinformatics, we provided a filter for what downstream molecules undertook the changes of the above cardiogenic gene expressions, thereby causing the phenotypes of heart tube formation in the presence of ZnO NPs (Figure 7). The results indicated that there were significantly decreased expressions of MYL2 and CSRP3, which are indispensable for myocardial differentiation (Li et al. 2019). Previous studies have also shown that mutations (missense, small insertions, and deletions) in CSRP3 are associated with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) in humans (Bos et al. 2006; Mohapatra et al. 2003). MYL2 null hearts manifested an embryonic form of dilated cardiomyopathy and resulted in heart failure with reduced ventricular ejection fraction (Chen et al. 1998). Wnt3a could inhibit the expression of early cardiac genes in the cardiac crescent, including NKX2.5 and GATA4 (Tian, Cohen, and Morrisey 2010). Hence, it is understandable that ZnO NPs exposure led to abnormal cardiogenesis, which might result from the inhibition of CSRP3 and MYL2. Notably, CSRP3 and MYL2 might also involve in the high-dose ZnO NPs-induced heart tube malformation since Fer-1 (an inhibitor of ferroptosis) administration significantly rescued the expressions of these key genes related to early cardiogenesis. These results certainly confirmed that ferroptosis played an important role in the pathological development of heart tube malformation in the context of ZnO NPs exposure (Supplementary Figure 5,11).
LncRNA-MYL2-2 and miR-124-3p Are Associated with Perioperative Neurocognitive Disorders in Patients after Cardiac Surgery
Published in Journal of Investigative Surgery, 2021
Qiu-Xia Xiao, Chun-Xia Cheng, Rui Deng, Qing Liu, Ying-Bo Ren, Li He, Feng-Xu Yu, Ying Zhang
Long non-coding RNAs (lncRNAs) were ever considered as “noise” without biological functions in the gene transcription process [14]. However, with the advent of abundant in-depth studies, it was found that lncRNAs can extensively participate in important biological processes of the body in the form of non-coding RNA, such as interaction with proteins, the formation of endogenous siRNA, regulation of mRNA variant splicing, chromatin remodeling and histone remodeling, adsorption of miRNA [15–17]. Among these, acting as a microRNA sponge to competitively binding miRNA was an important way for lncRNA to regulate transcription [18, 19]. LncRNA-PAGBC could promote tumor growth and metastasis of GBC cells through adsorbing miR-133b and miR-511 to activate the AKT/mTOR pathway [20]. In our previous research, we analyzed lncRNAs and mRNAs differential expression profile between PND and non-PND patients using microarray analysis and found lncRNA-MYL2-2 differentially expressed between PND and non-PND patients using bioinformatics technology [21]. Nevertheless, there were few large scale clinical investigations about the relation of lncRNA-MYL2-2 and PND.