Takasaki I, Chobanian A V, Sarzani R, Brecher P
Department of Medicine, Boston University School of Medicine, Massachusetts 02118.
J Biol Chem. 1990 Dec 15;265(35):21935-9.
Interactions between extracellular fibronectin and vascular cells are thought to influence the phenotype of those cells. To determine if changes in fibronectin expression accompany the phenotypic changes of vascular tissue characteristic of experimental hypertension, steady state mRNA levels for fibronectin were determined in aortae of normotensive and hypertensive rats. A 3-6-fold increase in fibronectin mRNA was observed in aortic tissue of hypertensive rats following 3 weeks of treatment with deoxycorticosterone and salt, whereas if rats were treated only with deoxycorticosterone or salt alone, no changes occurred. The changes were reversed by normalization of blood pressure. The increases observed were localized to aorta and not to the periaortic tissue. Angiotensin II infusion using osmotic minipumps also caused an increase in fibronectin expression. Age-dependent increases in aortic fibronectin mRNA occurred in several rat strains, and the combined effects of hypertension and aging were greater than either variable alone. A clear distinction between the expression of fibronectin mRNA and that for collagen or tropoelastin were found in hypertensive and aging models. Aortic fibronectin was also increased in the hypertensive rats as determined by Western blot analysis. The findings indicate that elevation in blood pressure increases fibronectin expression in rat aorta and suggest that such changes may influence the aortic cellular responses to hypertension.
细胞外纤连蛋白与血管细胞之间的相互作用被认为会影响这些细胞的表型。为了确定纤连蛋白表达的变化是否伴随实验性高血压特征性血管组织的表型变化，在正常血压和高血压大鼠的主动脉中测定了纤连蛋白的稳态mRNA水平。在用脱氧皮质酮和盐治疗3周后，高血压大鼠的主动脉组织中观察到纤连蛋白mRNA增加了3至6倍，而如果大鼠仅用脱氧皮质酮或盐单独治疗，则没有变化。血压正常化可逆转这些变化。观察到的增加局限于主动脉，而不是主动脉周围组织。使用渗透微型泵输注血管紧张素II也会导致纤连蛋白表达增加。几种大鼠品系的主动脉纤连蛋白mRNA随年龄增长而增加，高血压和衰老的联合作用大于单独的任何一个变量。在高血压和衰老模型中发现纤连蛋白mRNA与胶原蛋白或原弹性蛋白的表达有明显区别。通过蛋白质印迹分析确定，高血压大鼠的主动脉纤连蛋白也增加。这些发现表明血压升高会增加大鼠主动脉中纤连蛋白的表达，并表明这种变化可能会影响主动脉细胞对高血压的反应。
