Inhibition of MYOCD/SRF‑mediated CDKN1A Transcription Attenuates Airway Remodeling in OVA-induced Asthmatic Mice
Description
We hypothesized that the MYOCD/SRF transcriptional complex drives asthmatic airway remodeling by directly upregulating the cell cycle regulator CDKN1A, and that targeted pharmacological blockade of MYOCD would mitigate these pathological structural changes. Our dataset comprises pulmonary function metrics, histological morphometry, transcriptomic profiles (RNA-seq), and multidimensional molecular validations (RT-qPCR, Western blot, and ChIP-qPCR). These data were meticulously gathered from an in vivo C57BL/6 murine asthma model (OVA-sensitized and challenged). The experimental design included a vehicle control, an untreated asthma model, and a treatment group administered the specific MYOCD inhibitor CCG-100602. Researchers can interpret and utilize this dataset as robust molecular evidence defining the specific downstream regulatory network of MYOCD in airway pathology. Furthermore, the data provide a foundational reference for evaluating the MYOCD/SRF/CDKN1A signaling axis as a viable, precise therapeutic target for the clinical treatment of refractory asthma.