PDGF-BB, a key member of the PDGF family, is a peptide growth factor with diverse biological functions. In vitro studies have demonstrated that venous VSMCs are smaller, spindle-shaped, and exhibit enhanced proliferative and migratory potential. Commonly used vascular grafts in CABG include the left internal mammary artery (LIMA), radial artery (RA), and great saphenous vein (GSV). Check if you have access through your login credentials or your institution to get full access on this article. If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Authors of the article cited in the comment will be invited to reply, as appropriate. ELetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Expression and promoter analysis of a highly restricted integrin alpha gene in vascular smooth muscle.
For the very first time, agent of the Special Operations Executive (SOE), Harry Hawker steps out of the shadows as the lead protagonist While Sniper Elite 5 included updates set in Vichy France, the team decided to make a standalone game set in this location because the team "felt that there was much more to explore". The game retained the same gameplay systems, though the team added some new features, such as a new grenade type and a new timed-based mode. Once in Amiens, Hawker finds out that when he finishes his mission by trapping the Zugwerfers for an RAF bombing, he will not be able to escape in time. The dam from the first mission is being repaired, however, one of the crashed RAF bombers had a bouncing bomb, which the Germans are studying.
Changes in retardation with time when the chemical reagent was applied to the cell to alter the cellular contraction state. Under the assumption that the refractive index stays constant, retardation measurements provide information on the mechanical state. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.
Virgin And Photo-degraded Microplastics Induce The Activation Of Human Vascular Smooth Muscle Cells
This value is larger than the cell retardation measured in the current study, approximately 0.3 nm (Fig. 4h), implying that changes in cell retardation would not be detected in aortic tissue. According to our previous study31, the retardation of aortic tissue with a thickness of 100 µm is approximately 30 nm. This study demonstrates that retardation measurement is useful for evaluating the cell phenotype in VSMCs. Generally, SFs in cells dynamically change their position and structure on this time scale. Figure 2b of the present study shows that retardation increased mainly in the central region upon calyculin A application, implying that retardation is increased by SF contraction. (d–f) Changes in (d) cell retardation, RetCell; (e) cell area, ACell; and (f) total cell retardation, RetCellTotal, with time. (a–c) Typical time-lapse images of retardation of single cells after application of (a) DMEM (control), (b) calyculin A, and (c) Y solution.
Buffer solutions—such as the University of Wisconsin solution, TiProtec, and He solution—can better maintain ion homeostasis and physiological pH. These solutions provide superior protection of endothelial structure and function compared to AWB and normal saline (93). The proposed protective mechanisms include the preservation of eNOS activity, which is abundantly expressed in the adventitia, and the retention of perivascular adipose tissue markers such as leptin and adiponectin (85, 86). These approaches provide a diversified portfolio for improving vein graft patency. Further elucidation of their roles may not only deepen our understanding of IH but also provide theoretical foundations and therapeutic targets for developing effective intervention strategies. To facilitate comparison and provide an integrated overview of the evidence discussed above, representative studies describing non-coding RNAs-mediated regulation of VSMCs phenotypic switching, including molecular targets and functional consequences, are summarized in Table 2. These molecules participate in the regulation of VSMCs phenotypic switching through intricate molecular mechanisms and play essential roles in the onset and progression of cardiovascular diseases (Figure 2).
Another significant structural change of vascular aging is the calcification of tunica intima and tunica media. All of them significantly reduced VSMCs stiffness in vivo and in vitro, confirming the possibility of targeting cytoskeletal protein junctions for the treatment of vascular sclerosis . At the same time, ECM degradation also facilitated VSMCs migration and neointimal formation. Contractile VSMCs spontaneously modify their phenotype instantaneously to synthetic phenotype when vascular damage occurs. The interaction between VSMCs and other cell types (such as endothelial cells, macrophages, and lymphocytes) in the complex environment of vascular diseases may involve Notch pathway to regulate VSMCs phenotype, which needs to be further investigated. Given the diversity of miRNAs involved in VSMCs phenotype regulation, we believe that manifold miRNAs that potentially regulate VSMCs phenotype switching remain undiscovered. In general, miRNAs that inhibit VSMCs ossification include miR-542-3p , miR-133a , miR-135a miR-204 , and miR-223-3p , all of which regulate osteogenic switching of VSMCs by directly binding to osteogenic genes or related transcription factors. Early studies have established the importance of miRNAs in vascular calcification, and miRNAs can serve as vascular calcification markers .
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In the PKG-independent pathway, 6-aminonicotinamide can directly stimulate the expression of MYOCD/miR-143 and downregulate the synthetic phenotype-responsive SRF-ELK1 complex to maintain the contractile phenotype. HnRNPA1 is a key regulator of PKM2 mRNA splicing, which can promote PKM2 expression and glycolysis. PKM2 is a key enzyme in the last step of glycolysis, converting phosphoenolpyruvate to pyruvate and supplying ATP . Acetyl CoA and citrate produced by glycolysis provide fuel for de novo fatty acid synthesis . At the same time, upregulation of PFKFB3 builds a carbon atom-sharing bridge between glycolysis and fatty acid synthesis. Metabolic reprogramming of plaques provide clues to changes in the metabolic pattern of cells within the plaque. In high-risk plaques, glycolysis and pentose phosphate pathway (PPP) are enhanced, fatty acid oxidation (FAO) is reduced, and amino acid anaplerosis is increased 5,6,7. Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. All claims expressed in this article are solely those ooosch casino login of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. This approach offers the potential for sustained inhibition and even regression of IH. This shift provides a scientific basis for the advancement of cardiovascular disease therapies. Currently, the primary pharmacological agents include microtubule stabilizers (e.g., paclitaxel-based drugs) and mTOR signaling inhibitors (e.g., rapamycin-based drugs). EDIs, which are buffer solutions developed based on the GALA formula (containing reduced glutathione, L-ascorbic acid, and L-arginine), exhibit antioxidant properties, scavenge free radicals, and support eNOS activity (95, 96).
2 Intimal Hyperplasia
Several mouse lines for cell lineage tracing have been developed and used for studying VSMC phenotypic switching. In vitro studies have shown that VSMCs can be de‐differentiated to a myofibroblast‐like VSMC state by stimulating VSMCs with platelet‐derived growth factor and transforming growth factor‐β.21, 54 In vivo studies have suggested that myofibroblast‐like VSMCs are derived from a subset of tenascin C VSMCs recruited from the tunica media.55 Hao et al found a subpopulation of VSMCs in the intima of human atherosclerotic lesions that had reduced or completely lost expression of MYH11 and SMTN, and displayed characteristics of myofibroblasts.50 The myofibroblast cell is phenotypically intermediate between fibroblasts and VSMCs.51 Mechanistically, the study of Pan et al14 suggests that cellular retinoic acid binding protein 2, a transducer of retinoic acid signaling, is a master regulator of vascular cell adhesion molecule 1 and lymphocyte antigen 6 family member C1. Mechanistically, studies have suggested that during atherogenesis, KLF4 mediates VSMC transition from the contractile phenotype to mesenchymal‐like phenotype cells.8, 13, 44 KLF4 inhibits the expression of sex‐determining region Y‐box 9, transient receptor potential cation channel subfamily V member 4, and S100 calcium‐binding protein B. Markers of the contractile phenotype include MYH11 (also known as smooth muscle myosin heavy chain 11), calponin, transgelin (also known as SM22α), myocardin, and α‐smooth muscle actin.11
Cholesterol‐induced phenotypic modulation of smooth muscle cells to macrophage/fibroblast‐like cells is driven by an unfolded protein response. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage‐like state after cholesterol loading. Low LAL (lysosomal acid lipase) expression by smooth muscle cells relative to macrophages as a mechanism for arterial foam cell formation. Contribution of intimal smooth muscle cells to cholesterol accumulation and macrophage‐like cells in human atherosclerosis. BMAL1 modulates smooth muscle cells phenotypic switch towards fibroblast‐like cells and stabilizes atherosclerotic plaques by upregulating YAP1.
Sorry, a shareable link is not currently available for this article. Changes in the retardation of cells treated with contraction and relaxation chemicals against controls were evaluated at each time point using Steel’s test. At each time point, the cell area, ACell, was measured by manually outlining the shape of the VSMCs in the phase contrast images. Because the retardation in background areas changed with time, a background image was taken just before imaging a cell. Retardations of passage 2 and 12 cells were compared because lower passage VSMCs have a contractile phenotype, while higher passage VSMCs dedifferentiate towards the synthetic phenotype39. VSMCs with the contractile phenotype show a higher retardation than those with the synthetic phenotype, suggesting that retardation can be used to evaluate VSMC phenotype.
In recent years, the rapid advancement of single-cell and spatial transcriptomics technologies has provided unprecedented spatiotemporal resolution for deciphering the dedifferentiation trajectories of VSMCs. These findings highlight the potential of folic acid and β‑aminoisobutyric acid to regulate VSMC phenotype by balancing amino acid metabolism and inflammation. Folic acid is a key regulator of nucleotide synthesis and methylation reactions. As atherosclerotic plaque formation and lipid deposition intensify, lipid abnormalities progressively emerge as key regulators of mid-to-late-stage phenotypic remodeling. Concurrently, glycolytic byproduct lactate promotes VSMC dedifferentiation by stabilizing HIF-1α, reinforcing the synthetic phenotype. Enhanced glucose metabolism promotes lipid synthesis and activates amino acid metabolism; disrupted lipid metabolism, in turn, negatively regulates glycolysis and amino acid utilization via ROS and ER stress, while amino acid metabolism provides compensatory substrates for impaired glucose and lipid metabolism during energy deficiency.
