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Last update 08 May 2025

MYOCD

Last update 08 May 2025

Basic Info

Synonyms

MYCD, myocardin, MYOCD

Introduction

Smooth muscle cells (SM) and cardiac muscle cells-specific transcriptional factor which uses the canonical single or multiple CArG boxes DNA sequence. Acts as a cofactor of serum response factor (SRF) with the potential to modulate SRF-target genes. Plays a crucial role in cardiogenesis, urinary bladder development, and differentiation of the smooth muscle cell lineage (myogenesis) (By similarity). Positively regulates the transcription of genes involved in vascular smooth muscle contraction (By similarity).

Drugs associated with MYOCD

MYOCD/ASCL1 Gene Therapy (Tenaya Therapeutics)

Target

ASCL1 x MYOCD

Mechanism

ASCL1 modulators [+1]

Active Org.

Tenaya Therapeutics, Inc.

Originator Org.

Tenaya Therapeutics, Inc.

Active Indication

Heart Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MYOCD

100 Translational Medicine associated with MYOCD

0 Patents (Medical) associated with MYOCD

750

Literatures (Medical) associated with MYOCD

15 Apr 2025·Circulation

Novel Directly Reprogrammed Smooth Muscle Cells Promote Vascular Regeneration as Microvascular Mural Cells

Article

Author: Chu, Nakhyung ; Han, Ji Woong ; Oh, Jee Eun ; Jung, Cholomi ; Kim, Kyung Hee ; Kim, Sangsung ; Lee, Eun Jig ; Yoon, Young-sup ; Nam, Young-Jae ; Dang, Chaewon ; Kim, Jaehyun ; Lee, Sangho ; Bae, Seongho ; Lee, Shin-Jeong

BACKGROUND:Although cell therapy has emerged as a promising approach to promote neovascularization, its effects are mostly limited to capillaries. To generate larger or more stable vessels, layering of mural cells such as smooth muscle cells (SMCs) or pericytes is required. Recently, direct reprogramming approaches have been developed for generating SMCs. However, such reprogrammed SMCs lack genuine features of contractile SMCs, a native SMC phenotype; thus, their therapeutic and vessel-forming potential in vivo was not explored. Therefore, we aimed to directly reprogram human dermal fibroblasts toward contractile SMCs (rSMCs) and investigated their role for generating vascular mural cells in vivo and their therapeutic effects on ischemic disease.METHODS: We applied myocardin and all- trans retinoic acid with specific culture conditions to directly reprogram human dermal fibroblasts into rSMCs. We characterized their phenotype as contractile SMCs through quantitative reverse-transcriptase polymerase chain reaction, flow cytometry, and immunostaining. We then explored their contractility using a vasoconstrictor, carbachol, and through transmission electron microscope and bulk RNA sequencing. Next, we evaluated whether transplantation of rSMCs improves blood flow and induces vessel formation as mural cells in a mouse model of hindlimb ischemia with laser Doppler perfusion imaging and histological analysis. We also determined their paracrine effects. RESULTS: Our novel culture conditions using myocardin and all- trans retinoic acid efficiently reprogrammed human dermal fibroblasts into SMCs. These rSMCs displayed characteristics of contractile SMCs at the mRNA, protein, and cellular levels. Transplantation of rSMCs into ischemic mouse hind limbs enhanced blood flow recovery and vascular repair and improved limb salvage. Histological examination showed that vascular density was increased and the engrafted rSMCs were incorporated into the vascular wall as pericytes and vascular SMCs, thereby contributing to formation of more stable and larger microvessels. Quantitative reverse-transcriptase polymerase chain reaction analysis revealed that these transplanted rSMCs exerted pleiotropic effects, including angiogenic, arteriogenic, vessel-stabilizing, and tissue regenerative effects, on ischemic limbs. CONCLUSIONS: A combination of myocardin and all- trans retinoic acid in defined culture conditions efficiently reprogrammed human fibroblasts into contractile and functional SMCs. The rSMCs were shown to be effective for vascular repair and contributed to neovascularization through mural cells and various paracrine effects. These human rSMCs could represent a novel source for cell-based therapy and research.

01 Apr 2025·Acta Pharmacologica Sinica

Colchicine reduces neointima formation and VSMC phenotype transition by modulating SRF-MYOCD activation and autophagy

Article

Author: Dong, Liang ; Zhu, Wen-Ya ; Zhu, Meng-Meng ; Ma, Chuan-Rui ; Ma, Li-Kun ; Chen, Yuan-Li ; Ma, Hui ; Zhang, Bu-Chun ; Yang, Xiao-Xiao ; Wang, Sheng-Nan

Vascular smooth muscle cell (VSMC) phenotype transformation significantly contributes to vascular intimal hyperplasia. However, effective preventive and therapeutic measures are lacking. Colchicine, a binary alkaloid derived from Colchicum autumnale, is traditionally used for treating inflammatory diseases. Its role in neointima formation is not fully understood. Here, we investigated the role of colchicine in vascular intimal hyperplasia. We found that colchicine significantly reduced vascular intimal hyperplasia in an animal model at 7, 14, and 28 days post carotid artery ligation and increased the number of contractile-phenotype VSMCs (SMA-positive cells) in the neointimal areas. In vitro experiments demonstrated that colchicine facilitated the transition of VSMCs from a proliferative phenotype to a contractile phenotype. Additionally, colchicine attenuated PDGF-BB-induced phenotypic conversion and upregulated the expression of serum response factor (SRF) and myocardin (MYOCD). Further molecular mechanistic studies revealed that colchicine inhibited the expression of forkhead box protein O3A (FOXO3A) to increase the activation of the SRF‒MYOCD complex. FOXO3A can bind to MSX1/2, thereby inhibiting the expression of SRF-MYOCD and contractile genes. Moreover, colchicine maintains vascular homeostasis and stabilizes the contractile phenotype by affecting the expression of autophagy-related genes (LC3II, p62, and Beclin-1) induced by FOXO3A. Additionally, colchicine inhibited monocyte/macrophage infiltration and inflammatory cytokine expression. In summary, this study suggests that colchicine inhibits vascular intimal hyperplasia by modulating FOXO3A-mediated SRF-MYOCD activation and autophagy, providing new insights for future therapeutic approaches targeting occlusive vascular diseases.

20 Mar 2025·Nan fang yi ke da xue xue bao = Journal of Southern Medical University

[The splicing factor HNRNPH1 regulates Circ-MYOCD back-splicing to modulate the course of cardiac hypertrophy].

Article

Author: He, Wenxia ; Ai, Tianhong ; Song, Xiaowei ; Hu, Shuting ; Huang, Zhuo ; Cai, Rui

OBJECTIVESTo explore the mechanism of Circ-MYOCD back-splicing and its regulatory role in myocardial hypertrophy.METHODSSanger sequencing and RNase R assays were performed to verify the circularity and stability of Circ-MYOCD, whose subcellular distribution was determined by nuclear-cytoplasmic fractionation. Bioinformatics analysis and mass spectrometry from pull-down assays were conducted to predict the RNA-binding proteins (RBPs) interacting with Circ-MYOCD. In rat cardiomyocytes H9C2 cells, the effects of HNRNPH1 and HNRNPL knockdown and overexpression on Circ-MYOCD back-splicing were evaluated. In a H9C2 cell model of angiotensin II (Ang II)-induced myocardial hypertrophy, the expression of HNRNPH1 was detected, the effects of HNRNPH1 knockdown and overexpression on progression of myocardial hypertrophy were assessed, and the regulatory effect of HNRNPH1 on Circ-MYOCD back-splicing was analyzed.RESULTSSanger sequencing confirmed that the junction primers could amplify the correct Circ-MYOCD sequence. RNase R and nuclear-cytoplasmic fractionation assays showed that Circ-MYOCD was stable and predominantly localized in the cytoplasm. Bioinformatics analysis and mass spectrometry from the Circ-MYOCD pull-down assay identified HNRNPH1 and HNRNPL as the RBPs interacting with Circ-MYOCD. In H9C2 cells, HNRNPH1 knockdown significantly enhanced while its overexpression inhibited Circ-MYOCD back-splicing; HNRNPH1 overexpression obviously increased the expressions of myocardial hypertrophy markers ANP and BNP, while its knockdown produced the opposite effect. In Ang II-induced H9C2 cells, which exhibited a significant increase of HNRNPH1 expression and increased expressions of ANP and BNP, HNRNPH1 knockdown obviously increased Circ-MYOCD expression, decreased MYOCD expression and lowered both ANP and BNP expressions.CONCLUSIONSHNRNPH1 regulates Circ-MYOCD back-splicing to influence the progression of myocardial hypertrophy.

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MYOCD

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