FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4207014793> ?p ?o ?g. }

• W4207014793 abstract "Dear Editor, The expression of myosin heavy chain 10 (MYH10) in atherosclerosis (AS) was positively correlated with the number of vascular smooth muscle cells (VSMCs), which were negatively related to the AS measured by intima-media thickness (IMT). MYH10 might be a potential biomarker for clinical AS, which was the formation of fibrous fatty lesions in the arterial wall. Over time, atherosclerotic plaques become more fibrotic.1 Advanced atherosclerotic plaques can invade arterial cavities, block blood flow, or form clots, resulting in tissue ischemia.2 Although some progress has been made in the treatment of AS, drugs and arterial interventional therapy cannot target the pathogenesis and progression of the disease, and there are risks of postoperative thrombosis and restenosis.3, 4 Because of the complexity of its pathogenesis, gene therapy is still in the stage of basic research and is still a serious challenge in modern medicine. VSMCs are one of the main cells that form the tissue structure of the vascular wall and maintain vascular tension. Studies have shown that the origin, phenotypic transformation, apoptosis, and calcification of VSMCs are closely related to AS.5 Some scholars believe that phenotypic transformation of VSMCs plays an important role in the formation of AS, and inhibition of phenotypic transformation of VSMCs has a protective effect on arteries.6 Under normal conditions, VSMCs in the arterial middle layer can express smooth muscle cell markers, such as myosin heavy chain 11 (MYH11), MYH9, MYH10, and α-smooth muscle actin (α-SMA), but the ability of VSMCs in the arterial middle layer with AS to express these markers is decreased.7 MYH10 (Myosin Heavy Chain 10) is a member of the Myosin superfamily.8 This protein represents a conventional non-muscle myosin. Myosin is an actin-dependent motor protein with a variety of functions, including regulation of cell division, cell movement, and cell polarity.9 However, the role of MYH10 and α-SMA in the development of AS remains unclear. Therefore, this study aims to explore the potential role of MYH10 in AS by weighted gene co-expression network analysis, gene set enrichment analysis, and analysis of AS-infiltrating immune cells. Furthermore, the mechanism of the interaction between MYH10 and α-SMA on AS was analysed through animal models of AS, and clinical specimen experiments. The hematoxylin-eosin staining (20×, 100×, 200×) results showed that the intima of the arterial sections in the normal group was smooth and muscle fibres were neatly arranged. However, for the clinical AS sample, muscle fibres were arranged irregularly, and the organizational structure is of evacuation (Figure 1A). The immunohistochemical assay (100×, 200×, 400×) results showed that the MYH10 was clearly expressed in the media of the arteries, and there were few expressions in the intima membrane in the normal group (The brown-yellow colour represents the expression of the MYH10 molecule, and the blue colour represents the nucleus). However, in the clinical AS samples, the MYH10 was down-expressed significantly in the media of arteries (Figure 1B). Furthermore, the immunofluorescence assay also manifested that compared with the normal group, the expression of MYH10 in the media of the arteries was lower in the clinical AS group, and there were very few expressions in the intima membrane (the red colour represents the expression of the MYH10 molecule, and the blue colour represents the nucleus; Figure 1C). Quantitative analysis of expression of MYH10 IHC-Score manifested that the expression of MYH10 was significantly lower in the clinical AS tissues than in the control group (Figure 1D). The RT-PCR results indicated that the relative expression level of MYH10 mRNA was significantly decreased in clinical AS artery compared with control artery tissue samples without AS (p < .05, Figure 1E). Western blotting analysis showed that the expression of MYH10 proteins was down-regulated in the clinical AS samples compared with the control group (Figure 1F). The immunohistochemistry and immunofluorescence assays (100×, 200×, 400×) showed that the expression of α-SMA protein in the clinical AS group was lower than that in the normal group. In immunohistochemistry, the brown-yellow colour represents the expression of the α-SMA molecule, and the blue colour represents the nucleus. The red colour represents the expression of the α-SMA molecule, and the blue colour represents the nucleus (Figure 2A,B). Through the Pearson rho analysis, there existed a strong negative relationship between the IMT and MYH10 (p = .001, R = -.532). The IMT was also negatively related to α-SMA (p < .001, R = −.4585). In addition, a strong relationship existed between α-SMA and MYH10 (p = .007, R = .454). A heatmap showed that there were strong correlations among the IMT, MYH10, and α-SMA (Figure 2C,D). The expression of MYH10 could predict the IMT sensitively and specifically (area under the curve [AUC] = .803, p < .001). Receiver operator characteristic curves were constructed to determine the effect of MYH10 and α-SMA on the IMT, with the degree of confidence judged by the AUC = .917 (p < .001, Figure 2E). Results of the cubic spline interpolation algorithm showed that MYH10 and α-SMA might be the high-risk warning indicator of IMT of the AS (Figure 2F). After training by neural network model, the best training performance is 0.036573 at epoch 3000 (Figure 3A). The relativity of the model (built by MYH10, α-SMA and IMT) is 0.92506 (Figure 3B). Furthermore, the model could be verified well, and there exists a tiny error between raw data and forecast data (Figure 3C,D). The above result could demonstrate that the joint effect of MYH10 and α-SMA would be predictive parameters of IMT in the clinical AS. Through the molecular docking study, the lowest binding energy of optimal complex conformation was −7.29 kcal/mol. The binding mode between the MYH10 and α-SMA was drawn (Figure 4A). Through the co-immunoprecipitation assay, the MYH10 and α-SMA were co-expressed in the artery (Figure 4B,C). In summary, the expression of MYH10 was positively correlated with the number of VSMCs (measured by α-SMA), which were negatively related to the AS measured by IMT. When MYH10 expression was low, the proliferation of VSMCs was decreased. Moreover, changes of VSMCs might promote the intima thickening and the formation of AS. The present study was funded by the National Key R&D Program of China (Grant no. 2020YFC2003000, 2020YFC2003001), Chinese Academy of Medical Sciences, CAMS Innovation Fund for Medical Sciences (Grant no. 2018-I2M-1-002), Central Health Research Project (W2017BJ11), and National Natural Science Foundation of China (Grant nos. 31271097 and 51672030). None. The authors declare that they have no conflict of interest. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article." @default.
• W4207014793 created "2022-01-26" @default.
• W4207014793 creator A5011492106 @default.
• W4207014793 creator A5024070173 @default.
• W4207014793 creator A5035184774 @default.
• W4207014793 creator A5038458885 @default.
• W4207014793 creator A5050030878 @default.
• W4207014793 creator A5058246479 @default.
• W4207014793 creator A5063337505 @default.
• W4207014793 creator A5072038986 @default.
• W4207014793 creator A5075019344 @default.
• W4207014793 creator A5085612180 @default.
• W4207014793 creator A5086886202 @default.
• W4207014793 creator A5090418801 @default.
• W4207014793 date "2022-01-01" @default.
• W4207014793 modified "2023-10-14" @default.
• W4207014793 title "A potential biomarker for clinical atherosclerosis: A novel insight derived from myosin heavy chain 10 promoting transformation of vascular smooth muscle cells" @default.
• W4207014793 cites W2126777451 @default.
• W4207014793 cites W2150949973 @default.
• W4207014793 cites W2274924551 @default.
• W4207014793 cites W2790654167 @default.
• W4207014793 cites W2809632591 @default.
• W4207014793 cites W2901056057 @default.
• W4207014793 cites W2941700485 @default.
• W4207014793 cites W3031940223 @default.
• W4207014793 cites W3103761932 @default.
• W4207014793 cites W4211134725 @default.
• W4207014793 doi "https://doi.org/10.1002/ctm2.672" @default.
• W4207014793 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35075787" @default.
• W4207014793 hasPublicationYear "2022" @default.
• W4207014793 type Work @default.
• W4207014793 citedByCount "1" @default.
• W4207014793 countsByYear W42070147932022 @default.
• W4207014793 crossrefType "journal-article" @default.
• W4207014793 hasAuthorship W4207014793A5011492106 @default.
• W4207014793 hasAuthorship W4207014793A5024070173 @default.
• W4207014793 hasAuthorship W4207014793A5035184774 @default.
• W4207014793 hasAuthorship W4207014793A5038458885 @default.
• W4207014793 hasAuthorship W4207014793A5050030878 @default.
• W4207014793 hasAuthorship W4207014793A5058246479 @default.
• W4207014793 hasAuthorship W4207014793A5063337505 @default.
• W4207014793 hasAuthorship W4207014793A5072038986 @default.
• W4207014793 hasAuthorship W4207014793A5075019344 @default.
• W4207014793 hasAuthorship W4207014793A5085612180 @default.
• W4207014793 hasAuthorship W4207014793A5086886202 @default.
• W4207014793 hasAuthorship W4207014793A5090418801 @default.
• W4207014793 hasBestOaLocation W42070147931 @default.
• W4207014793 hasConcept C104317684 @default.
• W4207014793 hasConcept C126322002 @default.
• W4207014793 hasConcept C185592680 @default.
• W4207014793 hasConcept C204241405 @default.
• W4207014793 hasConcept C2779395532 @default.
• W4207014793 hasConcept C2781197716 @default.
• W4207014793 hasConcept C2992686903 @default.
• W4207014793 hasConcept C502942594 @default.
• W4207014793 hasConcept C55493867 @default.
• W4207014793 hasConcept C6997183 @default.
• W4207014793 hasConcept C70721500 @default.
• W4207014793 hasConcept C71924100 @default.
• W4207014793 hasConcept C86803240 @default.
• W4207014793 hasConcept C95444343 @default.
• W4207014793 hasConceptScore W4207014793C104317684 @default.
• W4207014793 hasConceptScore W4207014793C126322002 @default.
• W4207014793 hasConceptScore W4207014793C185592680 @default.
• W4207014793 hasConceptScore W4207014793C204241405 @default.
• W4207014793 hasConceptScore W4207014793C2779395532 @default.
• W4207014793 hasConceptScore W4207014793C2781197716 @default.
• W4207014793 hasConceptScore W4207014793C2992686903 @default.
• W4207014793 hasConceptScore W4207014793C502942594 @default.
• W4207014793 hasConceptScore W4207014793C55493867 @default.
• W4207014793 hasConceptScore W4207014793C6997183 @default.
• W4207014793 hasConceptScore W4207014793C70721500 @default.
• W4207014793 hasConceptScore W4207014793C71924100 @default.
• W4207014793 hasConceptScore W4207014793C86803240 @default.
• W4207014793 hasConceptScore W4207014793C95444343 @default.
• W4207014793 hasFunder F4320321001 @default.
• W4207014793 hasIssue "1" @default.
• W4207014793 hasLocation W42070147931 @default.
• W4207014793 hasLocation W42070147932 @default.
• W4207014793 hasLocation W42070147933 @default.
• W4207014793 hasLocation W42070147934 @default.
• W4207014793 hasOpenAccess W4207014793 @default.
• W4207014793 hasPrimaryLocation W42070147931 @default.
• W4207014793 hasRelatedWork W1493591168 @default.
• W4207014793 hasRelatedWork W1541774345 @default.
• W4207014793 hasRelatedWork W1985441333 @default.
• W4207014793 hasRelatedWork W2024516096 @default.
• W4207014793 hasRelatedWork W2052034731 @default.
• W4207014793 hasRelatedWork W2069988633 @default.
• W4207014793 hasRelatedWork W2296993827 @default.
• W4207014793 hasRelatedWork W2350376131 @default.
• W4207014793 hasRelatedWork W2586762470 @default.
• W4207014793 hasRelatedWork W3087504962 @default.
• W4207014793 hasVolume "12" @default.
• W4207014793 isParatext "false" @default.
• W4207014793 isRetracted "false" @default.
• W4207014793 workType "article" @default.