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Quantification of Atherosclerosis in Mice
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Osteoglycin deficiency does not affect atherosclerosis in mice.

Javier Moncayo-Arlandi1, Alejandro López-García2, M Carmen Fernández2

  • 1Cardiovascular Genetics Centre, Biomedical Research Institut of Girona, Spain.

Atherosclerosis
|December 3, 2014
PubMed
Summary

The small leucine-rich proteoglycan Osteoglycin/Mimecan (OGN) does not impact atherosclerosis progression. Studies using double knockout mice showed no significant differences in lesion size or composition, indicating OGN is not a key factor in this disease.

Keywords:
ApoeKnockout mouseOsteoglycinSmall Leucine-Repeat Domain Protein

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Area of Science:

  • Cardiovascular Biology
  • Extracellular Matrix Research
  • Atherosclerosis Pathogenesis

Background:

  • Osteoglycin/Mimecan (OGN), a small leucine-rich proteoglycan, is found in blood vessels and influences extracellular matrix composition.
  • OGN plays a role in collagen fibrillogenesis and cytokine regulation.
  • Previous studies indicated OGN alterations in atherosclerotic lesions and effects on collagen in skin and cornea.

Purpose of the Study:

  • To investigate the role of OGN in the progression of atherosclerosis.
  • To determine if the absence of OGN affects atherosclerotic lesion development.
  • To utilize a double knockout mouse model for comprehensive analysis.

Main Methods:

  • Developed double Apoe(-/-)Ogn(-/-) knockout mice and compared them with Apoe(-/-)Ogn(+/+) mice.
  • Conducted comparative histomorphological and immunofluorescence studies of atherosclerotic lesions.
  • Analyzed Ogn transcript presence in wildtype and knockout mouse aortas.

Main Results:

  • Confirmed the presence of Ogn transcript in wildtype aorta and its absence in Ogn(-/-) mice.
  • Observed similar histomorphology, extracellular matrix composition, and cellular content in lesions of both double and single knockout groups.
  • Found no significant differences in lesion size, calcium deposit incidence, size, or distribution between Apoe(-/-)Ogn(-/-) and Apoe(-/-)Ogn(+/+) mice.

Conclusions:

  • The absence of Osteoglycin/Mimecan (OGN) does not influence the progression of atherosclerosis in mice.
  • The study did not reveal a significant role for OGN in the development or characteristics of atherosclerotic lesions.
  • Potential reasons for the lack of a phenotype in the double mutant mice are discussed.