Ask about this productRelated genes to: Myocd Blocking Peptide
- Gene:
- MYOCD NIH gene
- Name:
- myocardin
- Previous symbol:
- -
- Synonyms:
- MYCD
- Chromosome:
- 17p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-01
- Date modifiied:
- 2016-10-05
Related products to: Myocd Blocking Peptide
Related articles to: Myocd Blocking Peptide
- Mutations in BMP4 have been associated with malformations of the urinary tract in human patients. Genetic studies in mice have shown that these defects are linked to the expression of Bmp4 in the mesenchymal primordium of the ureter, where it acts as a critical signal for coordinated cytodifferentiation of the mesenchymal and epithelial tissues. Here, we used unbiased transcriptional profiling of ureters with genetic depletion of Bmp4 and pharmacological inhibition of BMP4 signaling to decipher the gene regulatory network controlled by BMP4 in the early ureter, focusing on transcription factors as possible drivers of cytodifferentiation. We show that in Bmp4-deficient ureters, expression of Grhl3, Msx2, Pparg, Trp63 and Foxa1 in the epithelial compartment, and of Gata6, Hopx, Id2, Id4, Myocd, Snai1 and Tbx18 in the mesenchymal primordium is reduced. Expression of Msx2, Pparg, Gata6, Id genes, Tbx18 and Snai1 requires direct BMP4 signaling input, whereas reduced expression of the other genes is likely due to secondary changes, including increased retinoic acid signaling. Conditional gene targeting of Smad4 revealed that BMP4-dependent activation of transcription factor genes is mediated in part by SMAD effectors in both ureteral tissues. Thus, our work links BMP4 (signaling) to known transcriptional regulators of ureteral cytodifferentiation and uncovers additional factors that may be relevant to this program. - Source: PubMed
Publication date: 2026/04/22
Deuper LenaHense NicolasBeckers AnjaThiesler HaukeMamo Tamrat MBergmann FlorianHildebrandt HerbertTrowe Mark-OliverKispert Andreas - Phenotypic switching of vascular smooth muscle cells (VSMCs) in the corpus spongiosum may contribute to abnormal urethral development in hypospadias, but the underlying molecular regulators remain unclear. This study aimed to identify hub genes associated with VSMCs phenotypic switching in the corpus spongiosum using RNA sequencing and Weighted Gene Co-expression Network Analysis (WGCNA), and to functionally characterize the top candidate gene . : Corpus spongiosum tissue samples were collected from seven patients with proximal hypospadias and five patients with urethral stricture (control group). The expression of the VSMCs contractile markers Calponin 1 and α-SMA, and the secretory marker OPN, was evaluated by qRT-PCR and Western blotting to assess VSMCs phenotypic state. RNA sequencing and Weighted Gene Co-expression Network Analysis (WGCNA) were performed to identify hub genes, which were then validated by qRT-PCR. Primary VSMCs were isolated from corpus spongiosum tissue and transduced with lentiviral vectors to either suppress or overexpress . Changes in VSMC marker expression and in key signaling pathways associated with phenotypic switching-specifically and -were analyzed using qRT-PCR and Western blotting. : In hypospadias tissue, the decreased expression of α-SMA and Calponin 1, together with increased OPN, indicated a shift in VSMCs from a contractile to a secretory phenotype. RNA-seq and WGCNA identified 11 differentially expressed genes, among which showed a marked downregulation in hypospadias samples. In control VSMCs, inhibition led to reduced α-SMA and Calponin 1, elevated OPN, and suppressed activity of and signaling. Conversely, overexpression in VSMCs from hypospadias samples restored α-SMA and Calponin 1 expression, decreased OPN, and enhanced and pathway activation. : VSMCs in the corpus spongiosum surrounding the urethral plate in hypospadias undergo a transition from a contractile to a secretory phenotype. emerges from unbiased transcriptomic screening as a key hub gene and functions as a critical regulator of this process, maintaining the contractile phenotype by modulating canonical and signaling. The axis may represent a central pathway linking VSMC phenotypic switching to abnormal vascular remodeling in hypospadias. - Source: PubMed
Publication date: 2025/12/23
Huang JiayaoXu ZihanHuang JiachengYin XiaoqinHuang YichenChen Fang - Vascular smooth muscle cell (VSMC) degeneration is a major mechanism underlying abdominal aortic aneurysm (AAA) formation. However, the upstream signaling pathways that converge on the transcriptional machinery to drive VSMC degeneration remain elusive. Here, we integrated single-nucleus (sn) multi-omics, chromatin immunoprecipitation (ChIP)-seq, and wet lab validation to identify transcriptional effectors of VSMC-MAPK14, which we previously reported to promote AAA. Compared with wild-type (WT) mice, VSMC-Mapk14 knockout (KO) mice displayed reduced VSMC degeneration, as evidenced by decreased expression of markers of endoplasmic reticulum stress, the unfolded protein response, fibrosis, and apoptosis, after 7 days of Ang II infusion. SnRNA-seq revealed increased VSMCs and reduced fibroblast and immune cell populations in KOs. Reclustering VSMCs revealed an increased proportion of contractile cluster and a reduced proportion of fibrotic cluster in KOs. The VSMC differentiation gene program and upstream pathways were upregulated, whereas degeneration pathways, including extracellular matrix remodeling, inflammation, and apoptosis, were downregulated in KO VSMCs. snATAC-seq and validation revealed increased serum response factor (SRF) motif activity and expression but reduced RUNX2 expression in KO VSMCs. Integrative analysis of snATAC-seq, ChIP-seq, and bulk RNA-seq identified the MYOCD/SRF/CArG triad as the driver of the contractile gene program following Mapk14 loss. We further found that the expression of Bcl2, a novel MYOCD/SRF/CArG target, was increased in Mapk14 KO VSMCs. Loss of Mapk14 attenuated MRTFA protein abundance via increased ubiquitin‒proteasome degradation, which was attributed to reduced USP10 protein expression. These findings reveal MAPK14-driven transcriptomic and epigenomic landscapes that promote VSMC degeneration by suppressing SRF/MYOCD/CArG while activating RUNX2 and MRTFA. Our study provides mechanistic insight into MAPK14-mediated VSMC degeneration and provides a basis for MAPK14-targeted therapeutic strategies for AAA. - Source: PubMed
Publication date: 2026/01/12
Wu XiaoliangWang ChunhuiIshimwe NestorZhang WeiDoja JaserShan ShengshuaiGe ChunyuSun YongZhao JinjingCastillo MicahSotonyi PeterGyurok GergoCsanyi GaborBryant W BartDong KunzheChen YabingVazquez-Padron RobertoMiano Joseph MLong Xiaochun - Vascular smooth muscle cells (VSMCs) are characterized by a considerable plasticity. Their phenotypic switch (from contractile to synthetic) plays a crucial role in the atherosclerotic process, explaining that numerous studies focus on this phenotypic transition. Thus, it is essential to use VSMCs that have been finely phenotyped for experimental purposes. The use of MOVAS cell line is suitable because, unlike primary cells, it is believed that these cells retain their phenotype and avoid cell senescence in culture. This study aimed to assess the phenotype of MOVAS cells over culture passages to ensure that they retained a contractile phenotype, before using them for further investigations. - Source: PubMed
Publication date: 2025/12/19
Cadoret LucileOkwieka AnaïsBerquand AlexandrePietrement ChristineGillery PhilippeJaisson Stephane - Nexilin F-actin binding protein (NEXN) is crucial for myocardial structural integrity, but its role in HCC progression is unclear. This study aimed to elucidate the role of NEXN in HCC. NEXN was weakly expressed in HCC, and its reduction correlated with poorer overall, disease-free, and progression-free survival. Overexpressing NEXN inhibited cell proliferation, colony formation, migration, and invasion , as well as tumor formation . NEXN overexpression downregulated the expression of mesenchymal markers and partially upregulated E-cadherin expression. Mechanistically, NEXN overexpression reduced β-catenin nuclear accumulation. Furthermore, by binding to MYOCD, NEXN co-regulated the EMT in HCC through the WNT/β-catenin signaling pathway. In conclusion, the diminished expression of NEXN interacts with MYOCD, influencing poor HCC prognosis by promoting EMT via the NEXN-MYOCD-β-catenin signaling axis. These findings provide a preclinical foundation for the development of metastasis-targeting inhibitors within the WNT pathway. - Source: PubMed
Publication date: 2025/11/14
Wu QiongLiu XueXu YingWu HuiXu Xi-FengHuang JieZhang BoYao Qing-Hua