The p300 Knockout MOVAS Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the MOVAS mouse vascular smooth muscle cell line. This cell line features a targeted disruption of the p300 gene, resulting in loss of p300 protein expression and providing a robust loss-of-function model for studying p300-dependent transcriptional regulation. The CRISPR/Cas9-mediated gene disruption enables precise interrogation of p300 function without the confounding effects of pharmacological inhibition or transient knockdown.
The MOVAS cell line is an immortalized mouse aortic smooth muscle cell line originally isolated from the thoracic aorta of C57BL/6 mice. These cells maintain key characteristics of vascular smooth muscle cells, including expression of smooth muscle ??-actin and capacity for contractile and synthetic phenotypes. The MOVAS line is widely used as a model system to investigate vascular smooth muscle cell biology, including maintenance of vascular tone, structural integrity, and pathological processes such as atherosclerosis and restenosis. Its well-characterized background makes it suitable for genetic manipulation and downstream functional assays.
p300 (EP300) functions as a transcriptional coactivator and histone acetyltransferase that catalyzes acetylation of histone H3 and H4 tails, relaxing chromatin structure and facilitating gene transcription. It also acetylates numerous non-histone proteins, including p53, NF-??B p65, GATA4, SMAD2/3, and STAT3. In vascular smooth muscle cells, p300 mediates transcriptional responses to upstream signals such as TGF-??, PDGF, EGF, and HIF-1?? under hypoxic conditions. p300 forms complexes with key transcription factors and cofactors, such as CREB, NF-??B, ??-catenin, CBP, and PCAF, integrating multiple signaling pathways including TGF-??/SMAD, Wnt/??-catenin, p53, NF-??B, and hypoxia signaling. Through these interactions, p300 drives the expression of genes involved in proliferation, migration, and phenotypic switching.
Knockout of p300 in MOVAS cells disrupts the transcriptional networks that regulate vascular smooth muscle cell plasticity and pathological remodeling. This model enables the dissection of p300??s role in mediating the switch from a contractile to a synthetic, pro-migratory phenotype, a hallmark of vascular diseases such as atherosclerosis, restenosis, and hypertension. By ablating p300, researchers can delineate its specific contributions to growth factor-induced signaling and chromatin remodeling, as well as its interplay with other acetyltransferases and deacetylases. The MOVAS p300 knockout line thus provides a powerful tool for studying the molecular mechanisms underlying vascular smooth muscle dysfunction.
This knockout cell line is suitable for a broad range of experimental applications, including western blotting, RT-qPCR, ChIP-qPCR, and immunofluorescence to validate p300 loss and assess downstream targets. Functional assays such as cell proliferation, scratch wound healing, transwell migration, and collagen gel contraction can quantify the impact on cell behavior. Additionally, reporter gene assays and drug sensitivity testing enable high-throughput screening of histone acetyltransferase inhibitors or other therapeutic compounds. Researchers investigating vascular calcification, transcription regulation, or signaling cross-talk will find this model invaluable. For further details, please contact Ascent Research.
