SMYD2 regulates vascular smooth muscle cell phenotypic switching and intimal hyperplasia via interaction with myocardin

Zhou, Yu; Sharma, Shaligram; Sun, Xiaonan; Guan, Xiaoqing; Hou, Yuning; Yang, Zhe; Shi, Hang; Zou, Ming-Hui; Song, Ping; Zhou, Jiliang; Wang, Shenming; Hu, Zuojun; Li, Chunying

doi:10.1007/s00018-023-04883-9

Cited by 3 publications

(3 citation statements)

References 72 publications

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“…Lysine demethylase 3A (KDM3A), previously known as JMJD1a, interacts with myocardin and demethylates H3K9me3, thus promoting the expression of contractile genes [69]. In addition, numerous histone modifiers have been identified to regulate contractile genes, including PR/SET domain 6 (PRDM6), SET and MYND domain containing 2 (SMYD2), SUV39H1, polycomb repressive complexes 2 (PRC2), and protein arginine methyltransferase 5 (PRMT5) (Table 1; Figures 1 and 2) [68,[71][72][73][74][75]78]. Although previous studies elucidated the intricate regulation of transcription and histone modification, the specific roles of chromatin remodelers in directly executing chromatin transformations require further investigation.…”

Section: Epigenetic and Transcriptional Regulation Of Vsmc Plasticity...mentioning

confidence: 99%

SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies

Liu,

Zhao,

Zhao

et al. 2024

Cells

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Mature vascular smooth muscle cells (VSMC) exhibit a remarkable degree of plasticity, a characteristic that has intrigued cardiovascular researchers for decades. Recently, it has become increasingly evident that the chromatin remodeler SWItch/Sucrose Non-Fermentable (SWI/SNF) complex plays a pivotal role in orchestrating chromatin conformation, which is critical for gene regulation. In this review, we provide a summary of research related to the involvement of the SWI/SNF complexes in VSMC and cardiovascular diseases (CVD), integrating these discoveries into the current landscape of epigenetic and transcriptional regulation in VSMC. These novel discoveries shed light on our understanding of VSMC biology and pave the way for developing innovative therapeutic strategies in CVD treatment.

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Section: Epigenetic and Transcriptional Regulation Of Vsmc Plasticity...mentioning

confidence: 99%

SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies

Liu,

Zhao,

Zhao

et al. 2024

Cells

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“…Notably, SMYD2 deletion significantly influences the expression of myocardin and other genes implicated in differentiation of VSMCs (Toghill et al, 2018). In this context, it was recently reported that SMYD2's ability to suppress VSMC hyperplasia and neointima formation is mediated by myocardin (Liang et al, 2022; Zhou et al, 2023).…”

Section: Molecular Basis Of Vsmc Phenotypic Switchmentioning

confidence: 99%

“…SMYD2, known for its roles in regulating carcinogenesis and inflammation, also plays a role in regulating VSMC behavior. For example, deletion of SMYD2 results in a significant increase in both proliferation and migration of VSMCs (Zhou et al, 2023). Conversely, overexpression of SMYD2 exerts a marked inhibitory effect PDGF-BB-induced proliferation and migration.…”

Section: Role Of Other Proteins In Vsmc Phenotypic Switchmentioning

confidence: 99%

Phenotypic switching of vascular smooth muscle cells in atherosclerosis, hypertension, and aortic dissection

Elmarasi,

Elmakaty,

Elsayed

et al. 2024

Journal Cellular Physiology

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Vascular smooth muscle cells (VSMCs) play a critical role in regulating vasotone, and their phenotypic plasticity is a key contributor to the pathogenesis of various vascular diseases. Two main VSMC phenotypes have been well described: contractile and synthetic. Contractile VSMCs are typically found in the tunica media of the vessel wall, and are responsible for regulating vascular tone and diameter. Synthetic VSMCs, on the other hand, are typically found in the tunica intima and adventitia, and are involved in vascular repair and remodeling. Switching between contractile and synthetic phenotypes occurs in response to various insults and stimuli, such as injury or inflammation, and this allows VSMCs to adapt to changing environmental cues and regulate vascular tone, growth, and repair. Furthermore, VSMCs can also switch to osteoblast‐like and chondrocyte‐like cell phenotypes, which may contribute to vascular calcification and other pathological processes like the formation of atherosclerotic plaques. This provides discusses the mechanisms that regulate VSMC phenotypic switching and its role in the development of vascular diseases. A better understanding of these processes is essential for the development of effective diagnostic and therapeutic strategies.

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Let’s make it personal: CRISPR tools in manipulating cell death pathways for cancer treatment

Bayat,

Nahand

2024

Cell Biol Toxicol

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Advancements in the CRISPR technology, a game-changer in experimental research, have revolutionized various fields of life sciences and more profoundly, cancer research. Cell death pathways are among the most deregulated in cancer cells and are considered as critical aspects in cancer development. Through decades, our knowledge of the mechanisms orchestrating programmed cellular death has increased substantially, attributed to the revolution of cutting-edge technologies. The heroic appearance of CRISPR systems have expanded the available screening platform and genome engineering toolbox to detect mutations and create precise genome edits. In that context, the precise ability of this system for identification and targeting of mutations in cell death signaling pathways that result in cancer development and therapy resistance is an auspicious choice to transform and accelerate the individualized cancer therapy. The concept of personalized cancer therapy stands on the identification of molecular characterization of the individual tumor and its microenvironment in order to provide a precise treatment with the highest possible outcome and minimum toxicity. This study explored the potential of CRISPR technology in precision cancer treatment by identifying and targeting specific cell death pathways. It showed the promise of CRISPR in finding key components and mutations involved in programmed cell death, making it a potential tool for targeted cancer therapy. However, this study also highlighted the challenges and limitations that need to be addressed in future research to fully realize the potential of CRISPR in cancer treatment. Graphical abstract Current application of CRISPR system in cancer therapy through a glance. A choosing the appropriate biological model for screening in vitro (using established cell lines, animal derived tumor cells, human derived tumor cells, stem cells or T cells), in vivo (using animal models which can harbor human derived tumor), or ex vivo (human/animal-derived organoids). B preparation of CRISPR gRNA library. C experimental design of CRISPR screening, identification of the desired gRNAs or phenotypic response. D CRISPR-Cas targeting of the identified targets, with Cas9 gene editing system (Knockout, base editing, prime editing), RNA modulation (modulation of RNA splicing, RNA base editing, RNA interference), and epigenomic edits and CRISPR interference/activation using dead Cas9 (dCas9) (Bock et al. 2022b)

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SMYD2 regulates vascular smooth muscle cell phenotypic switching and intimal hyperplasia via interaction with myocardin

Cited by 3 publications

References 72 publications

SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies

SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies

Phenotypic switching of vascular smooth muscle cells in atherosclerosis, hypertension, and aortic dissection

Let’s make it personal: CRISPR tools in manipulating cell death pathways for cancer treatment

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