system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: ARNTL Transcription Factors, Animals, Blood Pressure, Carotid Arteries, Carotid Artery Diseases, Cells, Cultured, Circadian Clocks, Elasticity, Endothelial Cells, Extracellular Matrix, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Matrix Metalloproteinase Inhibitors, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Mice, Mutant Strains, Myocytes, Smooth Muscle, Period Circadian Proteins, Phenylalanine, Protease Inhibitors, Thiophenes, Time Factors, Ultrasonography, Doppler, Pulsed.
user
Do matrix metalloproteinase 2 and 9 dysfunction underlie vascular stiffness in circadian clock mutant mice? Context: To determine if elasticity in blood vessels is compromised in circadian clock-mutant mice (Bmal1-knockout [KO] and Per-triple KO) and if matrix metalloproteinases (MMPs) might confer these changes in compliance. High-resolution ultrasonography in vivo revealed impaired remodeling and increased pulse-wave velocity in the arteries of Bmal1-KO and Per-triple KO mice. In addition, compliance of remodeled arteries and naïve pressurized arterioles ex vivo from Bmal1-KO and Per-triple KO mice was reduced, consistent with stiffening of the vascular bed. The observed vascular stiffness was coincident with dysregulation of MMP-2 and MMP-9 in Bmal1-KO mice. Furthermore, inhibition of MMPs improved indexes of pathological remodeling in wild-type mice, but the effect was abolished in Bmal1-KO mice.
assistant
Circadian clock dysfunction contributes to hardening of arteries, which may involve impaired control of the extracellular matrix composition. Final Decision: yes