| First Author | Thompson JC | Year | 2018 |
| Journal | Atherosclerosis | Volume | 268 |
| Pages | 68-75 | PubMed ID | 29182988 |
| Mgi Jnum | J:331016 | Mgi Id | MGI:6869773 |
| Doi | 10.1016/j.atherosclerosis.2017.11.005 | Citation | Thompson JC, et al. (2018) Elevated circulating TGF-beta is not the cause of increased atherosclerosis development in biglycan deficient mice. Atherosclerosis 268:68-75 |
| abstractText | BACKGROUND AND AIMS: Vascular biglycan contributes to atherosclerosis development and increased biglycan expression correlates with increased atherosclerosis. However, mice deficient in biglycan have either no reduction in atherosclerosis or an unexpected increase in atherosclerosis. Biglycan deficient mice have systemically elevated TGF-beta, likely due to lack of sequestration of TGF-beta in the extracellular matrix. The purpose of this study was to determine if prevention of TGF-beta elevations in biglycan deficient mice affected atherosclerosis development. METHODS: Biglycan deficient mice were crossed to Ldlr deficient mice. Diabetes was induced via streptozotocin and all mice were fed a high cholesterol diet. Diabetic biglycan wild type and biglycan deficient Ldlr deficient mice were injected with the TGF-beta neutralizing antibody 1D11 or the irrelevant control antibody 13C4. RESULTS: Biglycan deficient mice had significantly elevated plasma TGF-beta levels, which was further increased by diabetes, and significantly increased atherosclerosis. There was a significant correlation between TGF-beta concentrations and atherosclerosis. However, despite nearly complete suppression of plasma TGF-beta levels in mice treated with the TGF-beta neutralizing antibody 1D11, there was no significant difference in atherosclerosis between mice with elevated TGF-beta levels and mice with suppressed TGF-beta levels. CONCLUSIONS: The increased atherosclerosis in biglycan deficient mice does not appear to be due to elevations in TGF-beta. |
