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(Circulation. 2006;114:I-200 – I-205.)
© 2006 American Heart Association, Inc.

Myocardial Protection and Vascular Biology

Increased Collagen Deposition and Elevated Expression of Connective Tissue Growth Factor in Human Thoracic Aortic Dissection

Xinwen Wang, MD, PhD; Scott A. LeMaire, MD; Li Chen, MS; Ying H. Shen, MD, PhD; Yehua Gan, MD, PhD; Heather Bartsch, MS; Stacey A. Carter, BA; Budi Utama, PhD; Hesheng Ou, MD, PhD; Joseph S. Coselli, MD; Xing Li Wang, MD, PhD

From the Section of Adult Cardiac Surgery (X.W., S.A.L.M., L.C., Y.H.S., Y.G., H.B., S.A.C., B.U., H.O., J.S.C., X.L.W.), Texas Heart Institute at St. Luke’s Episcopal Hospital, and the Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Tex, and the Department of Vascular Surgery (X.W.) First Teaching Hospital, China Medical University, Shenyang, China.

Correspondence to Dr. Xing Li Wang, MS NAB 2010, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. E-mail xlwang{at}bcm.tmc.edu

Background— Thoracic aortic dissection (TAD) is characterized by dysregulated extracellular matrix. Little is known about the alterations of collagen and stimulators of collagen synthesis, eg, connective tissue growth factor (CTGF), in patients with TAD. In this study, we examined their roles in TAD.

Methods and Results— Surgical specimens of the aortic wall of TAD patients (n=10) and controls (n=10) were tested for collagen types I and III and CTGF expression. When compared with controls, protein levels of type I and III collagen and CTGF were significantly increased by 3.2-, 3.7-, and 5.3-fold, respectively (P<0.05 for all). Similar patterns were shown in mRNA levels of type I and I2 collagen and CTGF. Using immunohistochemistry and trichrome staining, we also observed elevated levels of collagen in the aortic media and adventitia. Treatment with recombinant human CTGF increased collagen synthesis in cultured aortic smooth muscle cells in a dose- and time-dependent fashion, in which expression of collagens increased from 506±108 counts per minute to 2764±240 cpm by 50 ng/mL CTGF, and from 30±43 cpm to 429±102 cpm at 48 hours.

Conclusions— TAD patients exhibited significantly increased expression of aortic collagen types I and III as well as CTGF, which is likely to be responsible for the compromised aortic distensibility and systemic compliance. Because CTGF can increase collagen expression, CTGF may be a new target molecule in the pathogenesis and progression of TAD.

Key Words: aorta • collagen • defects • growth substances • muscle, smooth