| First Author | Sindermann JR | Year | 2002 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 283 |
| Issue | 6 | Pages | H2714-24 |
| PubMed ID | 12388294 | Mgi Jnum | J:135050 |
| Mgi Id | MGI:3790291 | Doi | 10.1152/ajpheart.00077.2002 |
| Citation | Sindermann JR, et al. (2002) Smooth muscle-specific expression of SV40 large TAg induces SMC proliferation causing adaptive arterial remodeling. Am J Physiol Heart Circ Physiol 283(6):H2714-24 |
| abstractText | To study the effects of enhanced smooth muscle cell (SMC) proliferation on arterial vessel geometry in the absence of vessel trauma, we developed a transgenic mouse model expressing SV40 large T antigen under control of the 2.3-kb smooth muscle-myosin heavy chain promoter. Transgenic mice studied at ages from 3 to 13 wk showed a 3.2-fold increase in arterial wall SMC density, with 28% of SMC exhibiting proliferative cell nuclear antigen staining, confirming enhanced SMC proliferation, which was accompanied by two- to threefold increases in arterial wall areas (P < 0.05). Remarkably, despite increased vessel wall mass, the lumen area was not compromised, but rather was increased. A tightly conserved linear relationship was found between arterial circumference and wall thickness with slopes of 0.036 for both transgenics (r = 0.93, P < 0.01) and controls (r = 0.77, P < 0.01), suggesting the hypothesis that the conservation of wall stress functions as a primary determinant of adaptive arterial remodeling. This establishes a new model of adaptive vessel remodeling occurring in response to a proliferative input in the absence of mechanical injury or primary flow perturbation. |
