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Relaxin and Matrix Metalloproteinase-9 in Angiotensin II-Induced Abdominal Aortic Aneurysms
Deborah A Howatt1, Maya Dajee2, Xiaojie Xie1,3
1Saha Cardiovascular Research Center, University of Kentucky.
Background:
This study determined whether relaxin or matrix metalloproteinase (MMP)-9 influences angiotensin II (AngII)-induced abdominal aortic aneurysms (AAA).
Methods And Results:
Male C57BL/6 or apolipoprotein E-/-mice were infused with AngII with or without relaxin. Relaxin did not influence AngII-induced AAA in either mouse strain. Infusion of AngII reduced, but relaxin increased, MMP-9 mRNA in macrophages. We then determined the effects of MMP-9 deficiency on AAA in apolipoprotein E-/-mice. MMP-9 deficiency led to AAA formation in the absence of AngII, and augmented AngII-induced aortic rupture and AAA incidence.
Conclusions:
MMP-9 deficiency augmented AngII-induced AAA.
Insights
Matrix metalloproteinase-9 (MMP-9) deficiency augmented angiotensin II-induced abdominal aortic aneurysms (AAA). Relaxin did not influence AAA, but affected MMP-9 expression in macrophages.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Biochemistry
Background:
- Abdominal aortic aneurysms (AAA) are a significant cause of mortality.
- The roles of relaxin and matrix metalloproteinase-9 (MMP-9) in AAA pathogenesis are not fully understood.
Purpose of the Study:
- To investigate the influence of relaxin and MMP-9 on angiotensin II (AngII)-induced AAA.
- To elucidate the specific mechanisms by which these factors affect AAA development.
Main Methods:
- AngII infusion in male C57BL/6 and apolipoprotein E knockout mice, with or without relaxin administration.
- Analysis of MMP-9 mRNA expression in macrophages.
- Assessment of AAA incidence and aortic rupture in MMP-9 deficient mice.
Main Results:
- Relaxin did not affect AngII-induced AAA formation in either mouse strain.
- AngII infusion decreased MMP-9 mRNA, while relaxin increased it in macrophages.
- MMP-9 deficiency led to AAA formation without AngII and worsened AngII-induced aortic rupture and AAA incidence.
Conclusions:
- MMP-9 deficiency significantly augmented AngII-induced AAA.
- These findings highlight a critical role for MMP-9 in AAA progression and suggest potential therapeutic targets.