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Updated: May 3, 2026
Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
Published on: May 16, 2025
Tenascin C protects aorta from acute dissection in mice
Taizo Kimura1, Kozoh Shiraishi2, Aya Furusho3
11] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine [3] Division of Cardiovascular Medicine, Medical Science for Control of Pathological Processes, Graduate School of Comprehensive Human Science, University of Tsukuba.
Tenascin-C (TNC) acts as a protective molecular damper, mitigating aortic stress. Its induction safeguards aortic integrity against acute hemodynamic and humoral challenges, preventing dissection.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Aortic Pathophysiology
Background:
- Acute aortic dissection (AAD) is a life-threatening condition.
- The role of the inflammatory response in AAD pathogenesis is recognized, but regulatory mechanisms remain unclear.
- Understanding protective pathways against aortic stress is crucial.
Purpose of the Study:
- To investigate the role of tenascin-C (TNC) as a protective mechanism against acute aortic stress.
- To elucidate the molecular pathways involved in TNC-mediated protection in the aorta.
- To determine the consequences of TNC deficiency in the context of aortic stress.
Main Methods:
- Induction of aortic stress using periaortic CaCl₂ and angiotensin II infusion in mice.
- Generation and utilization of tenascin-C (Tnc) gene-deleted mice.
- Assessment of aortic integrity, hemodynamic stress, inflammatory response, and TGFβ signaling.
Main Results:
- TNC induction was observed as a response to acute hemodynamic and humoral stress in the aorta.
- Tnc gene deletion sensitized mice to AAD development under aortic stress.
- AAD development in Tnc-deficient mice was associated with impaired TGFβ signaling, reduced extracellular matrix proteins, and heightened inflammation.
Conclusions:
- Tenascin-C functions as a stress-evoked molecular damper, crucial for maintaining aortic integrity.
- TNC mitigates destructive inflammatory responses and supports extracellular matrix homeostasis during acute aortic stress.
- Targeting TNC may offer a therapeutic strategy for preventing acute aortic dissection.
