SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation

Liang, Min; Cai, Zhaohua; Jiang, Yangjing; Huo, Huanhuan; Shen, Linghong; He, Ben

doi:10.3390/ijms232012637

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…Importantly, two main transcription factors that modulate expression of various genes implicated in phenotypic switch are serum response factor (SRF-2) and myocardin (Liang et al, 2022;Liu et al, 2023).…”

Section: Molecular Basis Of Vsmc Phenotypic Switchmentioning

confidence: 99%

“…Signaling messengers like cyclic AMP and cyclic GMP as well as inflammatory cues, metabolic pathways, and reactive oxygen species are also involved (Aboukhater et al, 2023; Al Attar et al, 2022; Anwar et al, 2017, 2018; Aramouni et al, 2023; Badran et al, 2019, 2020; Bhagani et al, 2020; Lincoln, 2006; Maaliki et al, 2019; Shaito et al, 2022; Wehbe et al, 2020). Importantly, two main transcription factors that modulate expression of various genes implicated in phenotypic switch are serum response factor (SRF‐2) and myocardin (Liang et al, 2022; Liu et al, 2023).…”

Section: Molecular Basis Of Vsmc Phenotypic Switchmentioning

confidence: 99%

See 1 more Smart Citation

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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Section: Molecular Basis Of Vsmc Phenotypic Switchmentioning

confidence: 99%

Section: Molecular Basis Of 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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show abstract

“…When Ang II receptor one is activated, Ang II can increase the stability of RhoGDI and promote the proliferation of VSMCs through SUMOylation ( Dai et al, 2019 ). Myocardin is a factor regulating the differentiation of smooth muscle cells (SMCs), which can be modified by SUMO1 to increase protein stability, and this process is reversibly regulated by SENP2, which is known to promote the phenotypic switching of VSMCs ( Liang et al, 2022 ).…”

Section: Regulatory Effects Of Sumoylation On Vascular Remodelingmentioning

confidence: 99%

The role of SUMOylation in the neurovascular dysfunction after acquired brain injury

Luo

Huang

et al. 2023

Front. Pharmacol.

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Acquired brain injury (ABI) is the most common disease of the nervous system, involving complex pathological processes, which often leads to a series of nervous system disorders. The structural destruction and dysfunction of the Neurovascular Unit (NVU) are prominent features of ABI. Therefore, understanding the molecular mechanism underlying NVU destruction and its reconstruction is the key to the treatment of ABI. SUMOylation is a protein post-translational modification (PTM), which can degrade and stabilize the substrate dynamically, thus playing an important role in regulating protein expression and biological signal transduction. Understanding the regulatory mechanism of SUMOylation can clarify the molecular mechanism of the occurrence and development of neurovascular dysfunction after ABI and is expected to provide a theoretical basis for the development of potential treatment strategies. This article reviews the role of SUMOylation in vascular events related to ABI, including NVU dysfunction and vascular remodeling, and puts forward therapeutic prospects.

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“…Full-length complementary cDNAs of GAS5 were synthesized and inserted into the expression vector pcDNA3.1 (Bioegene, Shanghai, China). NRCMs and HEK-293T for 48 h were chosen to establish stable overexpression and knockdown cell lines [45].…”

Section: Plasmid Construction and Cell Transfectionmentioning

confidence: 99%

LncRNA GAS5 Attenuates Cardiac Electrical Remodeling Induced by Rapid Pacing via the miR-27a-3p/HOXa10 Pathway

Wang

Chen

et al. 2023

IJMS

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Previous studies indicated long non-coding RNAs (lncRNAs) participated in the pathogenesis of atrial fibrillation (AF). However, little is known about the role of lncRNAs in AF-induced electrical remodeling. This study aimed to investigate the regulatory effect of lncRNA GAS5 (GAS5) on the electrical remodeling of neonatal rat cardiomyocytes (NRCMs) induced by rapid pacing (RP). RNA microarray analysis yielded reduced GAS5 level in NRCMs after RP. RT-qPCR, western blot, and immunofluorescence yielded downregulated levels of Nav1.5, Kv4.2, and Cav1.2 after RP, and whole-cell patch-clamp yielded decreased sodium, potassium, and calcium current. Overexpression of GAS5 attenuated electrical remodeling. Bioinformatics tool prediction analysis and dual luciferase reporter assay confirmed a direct negative regulatory effect for miR-27a-3p on lncRNA-GAS5 and HOXa10. Further analysis demonstrated that either miR-27a-3p overexpression or the knockdown of HOXa10 further downregulated Nav1.5, Kv4.2, and Cav1.2 expression. GAS5 overexpression antagonized such effects in Nav1.5 and Kv4.2 but not in Cav1.2. These results indicate that, in RP-treated NRCMs, GAS5 could restore Nav1.5 and Kv4.2 expression via the miR-27a-3p/HOXa10 pathway. However, the mechanism of GAS5 restoring Cav1.2 level remains unclear. Our study suggested that GAS5 regulated cardiac ion channels via the GAS5/miR-27a-3p/HOXa10 pathway and might be a potential therapeutic target for AF.

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SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation

Cited by 8 publications

References 36 publications

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

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

The role of SUMOylation in the neurovascular dysfunction after acquired brain injury

LncRNA GAS5 Attenuates Cardiac Electrical Remodeling Induced by Rapid Pacing via the miR-27a-3p/HOXa10 Pathway

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