This study investigates the role of hyaluronan synthase 3 (HAS3) in cardiac healing following myocardial infarction (MI). Using Has3(-/-) mice, the researchers demonstrated that HAS3 deficiency leads to impaired cardiac function, increased scar size, and a significant reduction in cardiac CD4(+) T cells, particularly Th1 and regulatory T cell subsets. The findings suggest that HAS3 is essential for mounting an effective T cell-mediated immune response during cardiac repair.
HAS3 deficiency impairs T cell activation and survival post-MI, resulting in compromised cardiac healing. The study highlights the critical role of HAS3 in modulating immune responses during cardiac repair.
Has3 Knockout (Has3(-/-)) mouse model, generated via targeted gene deletion to study the effects of HAS3 deficiency in vivo.
Myocardial infarction, Cardiac ischemia-reperfusion injury, T cell response, Hyaluronan synthase, Cardiac remodeling
Knockout mouse model, Targeted gene deletion, Immune cell profiling, Cardiac function assessment
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
