PubMed · 4952800
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H K Tsuji, J V Redington, J H Kay. 1967. Aortotomy closure.. https://doi.org/10.1016/s0003-4975(10)66709-4
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Biglycan and decorin are small dermatan sulfate-containing proteoglycans in the extracellular matrix of the artery wall. The dermatan sulfate chains are known to stimulate thrombin inhibition by heparin cofactor II (HCII), a plasma proteinase inhibitor that has been detected within the artery wall. The purpose of this study was to analyze the HCII-stimulatory activity of biglycan and decorin isolated from normal human aorta and atherosclerotic lesions type II through VI and to correlate activity with dermatan sulfate chain composition and structure. Biglycan and decorin from plaque exhibited a 24-75% and 38-79% loss of activity, respectively, in thrombin-HCII inhibition assays relative to proteoglycan from normal aorta. A significant negative linear relationship was observed between lesion severity and HCII stimulatory activity (r = 0.79, biglycan; r = 0.63, decorin; p < 0.05). Biglycan, but not decorin, from atherosclerotic plaque contained significantly reduced amounts of iduronic acid and disulfated disaccharides DeltaDi-2,4S and DeltaDi-4,6S relative to proteoglycan from normal artery. Affinity coelectrophoresis analysis of a subset of samples demonstrated that increased interaction of proteoglycan with HCII in agarose gels paralleled increased activity in thrombin-HCII inhibition assays. In conclusion, both biglycan and decorin from atherosclerotic plaque possessed reduced activity with HCII, but only biglycan demonstrated a correlation between activity and specific glycosaminoglycan structural features. Loss of the ability of biglycan and decorin in atherosclerotic lesions to regulate thrombin activity through HCII may be critical in the progression of the disease.
Proliferation of vascular smooth muscle cells (VSMC) is characteristic of restenosis following balloon angioplasty. We show here that a low concentration of a novel iron chelator, desferri-exochelin 772SM, reversibly arrests the growth of human VSMC in vitro, specifically in G(0)/G(1) and S phases. The lipophilic desferri-exochelin is effective more rapidly and at a 10-fold lower concentration than the nonlipophilic iron chelator deferoxamine. Treatment of growth-synchronized VSMC with the desferri-exochelin results in down-regulation of cyclin E/ Cdk2 and cyclin A/Cdk2 activity but does not affect the cyclin D/Cdk4/retinoblastoma phosphorylation pathway. Both DNA replication and RNA transcription are inhibited in exochelin-treated cells, but protein synthesis is not. The ability of desferri-exochelin 772SM to reversibly block the growth of VSMC in vitro with no apparent cytotoxicity suggests that the exochelin may be useful as a therapeutic agent to limit restenosis in injured vessels.
Respiratory symptoms are often present in infants with congenital cardiac anomalies, but the intrinsic pathology of the airway itself or external compression by abnormal vessels is frequently undetected before cardiac repair. We collected 12 patients with airway pathology from July 1996 to October 1998; all had definite diagnosis of lesions of the airway and its adjacent vessels by preoperative ultrafast computed tomography. Four had intrinsic pathology (one retrotracheal diverticulum, three tracheal stenosis) as well as external compression. Among them, six had complete vascular ring, four partial rings and three had bronchial compression by aneurysmal dilatation of branch pulmonary arteries. Simultaneous airway repair (one diverticulectomy, three patch tracheoplasty) and external decompression were performed in ten cases under cardiopulmonary bypass, nine of ten had simultaneous cardiac repair; the other two were done before cardiac repair. All survived except three. We concluded that ultrafast computed tomography is indispensable for definite diagnosis of airway and adjacent cardiovascular pathology. Mere repair of congenital cardiac defects without rectification of the airway and its adjacent structures is incompatible with survival.