Expression of platelet-derived growth factor B is upregulated in patients with thoracic aortic dissection

Objective: Thoracic aortic dissection (TAD) is a serious condition requiring urgent treatment to avoid catastrophic consequences. The inflammatory response is involved in the occurrence and development of TAD, possibly potentiated by platelet-derived growth factors (PDGFs). This study aimed to determine whether expression of PDGF-B (a subunit of PDGF-BB) was increased in TAD patients and to explore the factors responsible for its upregulation and subsequent effects on TAD. Methods: Full-thickness ascending aorta wall specimens from TAD patients (n = 15) and control patients (n = 10) were examined for expression of PDGF-B and its receptor (PDGFRB) and in terms of morphology, inflammation, and fibrosis. Blood samples from TAD and control patients were collected to detect plasma levels of PDGF-BB and soluble elastins. Results: Expression levels of PDGF-B, PDGFRB, and collagen I were significantly enhanced in ascending aorta wall specimens from TAD patients compared with controls. Furthermore, soluble elastic fragments and PDGF-BB were significantly increased in plasma from TAD patients compared with controls, and numerous irregular elastic fibers and macrophages were seen in the ascending aorta wall in TAD patients. Conclusions: An increase in elastic fragments in the aorta wall might be responsible for inducing the activation and migration ofmacrophages to injured sites, leading to elevated expression of PDGF-B, which in turn induces deposition of collagen, disrupts extracellularmatrix homeostasis, and increases the stiffness of the aorta wall, resulting in compromised aorta compliance. (J Vasc Surg 2018;68:3S-13S.) Clinical Relevance: The inflammatory response is known to play an important role in thoracic aortic dissection (TAD). We therefore examined the association between increased platelet-derived growth factor B (PDGF-B) expression and TAD. The results suggest that abnormal elastic fibers may result in increased levels of elastic fragments in the blood, thus inducing the activation and migration of macrophages to injured sites in the aorta, which in turn further exacerbates the degradation of elastic fibers. Activated macrophages involved in the local inflammatory response mediate the expression of PDGF-B, inducing collagen deposition, disrupting extracellular matrix homeostasis, and increasing stiffness of the aorta wall, with compromised aortic compliance. These results provide the basis for future studies of the relationship between PDGF-B and TAD and of PDGF-B as a potential therapeutic target in TAD patients.