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Bone disturbances and progression of atherosclerosis in ApoE knockout mice

1, 2, 3, 4, 5, 6, 7, 8

 

  1. Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon Academic Medical Centre, Lisbon, Portugal. diana.fernandes@gmail.com
  2. Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon Academic Medical Centre, Lisbon, Portugal.
  3. Rheumatology and Bone Metabolic Diseases Department, Centro Hospitalar Lisboa Norte, EPE - Hospital de Santa Maria, Lisbon Academic Medical Centre, Lisbon, Portugal.
  4. Cancer Research and Translational Medicine Research Unit, Faculty of Medicine, University of Oulu, Finland.
  5. Research Unit of Medical Imaging, Physics and Technology, Faculty of Medicine, University of Oulu, and Medical Research Center, University of Oulu, Finland.
  6. Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon Academic Medical Centre, Lisbon, and Rheumatology Department, Hospital Garcia de Orta, Almada, Portugal.
  7. CEDOC, EpiDoc Unit - Epidemiology of Chronic Diseases, Nova Medical School, Universidade Nova de Lisboa, Portugal.
  8. Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon Academic Medical Centre, Lisbon, and Rheumatology and Bone Metabolic Diseases Department, Centro Hospitalar Lisboa Norte, EPE - Hospital de Santa Maria, Lisbon Academic Medical Centre, Lisbon, Portugal.

CER16169
2023 Vol.41, N°9
PI 1746, PF 1753
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PMID: 36622103 [PubMed]

Received: 31/08/2022
Accepted : 14/11/2022
In Press: 04/01/2023
Published: 17/08/2023

Abstract

OBJECTIVES:
Epidemiological evidence supports a link between atherosclerosis and osteoporosis. These conditions might share common pathophysiological mechanisms, with inflammation being one of the hypotheses.Apolipoprotein E deficient mice (ApoE-/-) develop atherosclerotic lesions spontaneously, further aggravated by a high-fat diet. Their bone remodelling is also disturbed. We hypothesised that a proinflammatory state could be a common contributive factor for vessel and bone disturbances observed in this animal model.
METHODS:
We evaluated vessels and bones of ApoE-/- and control C57BL/6 (B6) female mice fed a high-fat diet in five time-points (8, 16, 20, 24 and 28 weeks of age) and quantified the development of atherosclerotic lesions, analysed gene expression of inflammatory and bone remodelling proteins (IL-1β, IL-6, IL-17A, TNF, RANKL, and OPG), measured serum bone turnover markers (P1NP and CTX-I), performed bone (L3-L4 vertebras) histomorphometric analysis and evaluated biomechanical properties of bones.
RESULTS:
We compared the outcomes of B6 and ApoE-/- groups at each time-point and, within each group, over time. Atherosclerotic lesions developed as previously described for ApoE-/- mice, but no significant differences were found in bone histomorphometry or biomechanical properties between ApoE-/- and B6 mice. Also, gene expression (either in bones or aortas) and serum biomarkers were similar in both groups. When considering over time evaluations we found that bone histomorphometry changes were similar between ApoE-/- and B6 mice, but CTX-I/P1NP ratio was significantly increased (meaning higher resorption than bone formation) in ApoE-/- as compared to B6 mice.
CONCLUSIONS:
Our study suggests that inflammation is not the principal driver for atherosclerosis progression and bone disturbances in this animal model.

DOI: https://doi.org/10.55563/clinexprheumatol/ydmqjl

Rheumatology Article

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