Disruption of the aortic elastic lamina and medial calcification share genetic determinants in mice.

نویسندگان

  • Susanna S Wang
  • Lisa J Martin
  • Eric E Schadt
  • Haijin Meng
  • Xuping Wang
  • Wei Zhao
  • Leslie Ingram-Drake
  • Martina Nebohacova
  • Margarete Mehrabian
  • Thomas A Drake
  • Aldons J Lusis
چکیده

BACKGROUND Disruption of the elastic lamina, as an early indicator of aneurysm formation, and vascular calcification frequently occur together in atherosclerotic lesions of humans. METHODS AND RESULTS We now report evidence of shared genetic basis for disruption of the elastic lamina (medial disruption) and medial calcification in an F(2) mouse intercross between C57BL/6J and C3H/HeJ on a hyperlipidemic apolipoprotein E (ApoE(-/-)) null BACKGROUND gene, known to mediate myocardial calcification. Using transgenic complementation, we show that Abcc6 also contributes to aortic medial calcification. CONCLUSIONS Our data indicate that calcification, though possibly contributory, does not always lead to medial disruption and that in addition to aneurysm formation, medial disruption may be the precursor to calcification.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

I-6: Remodelling Uterine Spiral Arteries inPregnancy

Background: During the first trimester of pregnancy the uterine spiral arteries that supply blood to the placenta are remodelled, creating heavily dilated conduits lacking maternal vasomotor control. To effect permanent vasodilatation, the internal elastic lamina and medial elastic fibres must be degraded. Failure of remodelling is a key characteristic of the pathological placenta and is though...

متن کامل

Aortic wall mechanics and composition in a transgenic mouse model of Marfan syndrome.

In Marfan syndrome, mutations of the fibrillin gene (FBN1) lead to aneurysm of the thoracic aorta, making the aortic wall more susceptible to dissection, but the precise sequence of events underlying aneurysm formation is unknown. We used a rodent model of Marfan syndrome, the mgR/mgR mouse (with mgR: hypomorphic FBN1 mutation), which underexpresses FBN1, to distinguish between a defect in the ...

متن کامل

Probucol nanostructured lipid carrier ameliorates elastase-induced abdominal aortic aneurysm in mice

Probucol (PB) is a drug commonly used for the treatment of hyperlipidemia and atherosclerosis. In our previous study, we have proved that PB can ameliorate abdominal aortic aneurysm (AAA) induced by elastase in mice through its anti-inflammatory and anti-oxidative effect. In this study, the water solubility and oral absorption of PB were improved by encapsulating PB into nanostructured lipid ca...

متن کامل

Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis

Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (c...

متن کامل

Intimomedial interface damage and adventitial inflammation is increased beneath disrupted atherosclerosis in the aorta: implications for plaque vulnerability.

BACKGROUND Atherosclerotic plaque progression is frequently accompanied by compensatory enlargement to preserve the lumen. These enlarging plaques develop features of vulnerability, however, leading to disruption and lumen obstruction. This complex transition from compensatory expansion to plaque disruption may not derive solely from progressive intimal disease. Concurrent changes at the intimo...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Circulation. Cardiovascular genetics

دوره 2 6  شماره 

صفحات  -

تاریخ انتشار 2009