Deep Vein Thrombosis Resolution Is Modulated by Monocyte CXCR2-Mediated Activity in a Mouse Model

DOI Web Site 被引用文献6件
  • Peter K. Henke
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Andrea Varga
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Sumit De
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • C. Barry Deatrick
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Jonathon Eliason
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Douglas A. Arenberg
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Pasu Sukheepod
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Porama Thanaporn
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Steven L. Kunkel
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Gilbert R. Upchurch
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.
  • Thomas W. Wakefield
    From the Section of Vascular Surgery, Jobst Vascular Research Laboratory, Department of Surgery (P.K.H., A.V., S.D., C.B.D., J.E., P.S., P.T., G.R.U., T.W.W.), the Division of Pulmonary Medicine, Department of Medicine (D.A.A.), and the Department of Pathology (S.L.K.), University of Michigan Medical School, Ann Arbor, Mich.

書誌事項

公開日
2004-06
DOI
  • 10.1161/01.atv.0000129537.72553.73
公開者
Ovid Technologies (Wolters Kluwer Health)

この論文をさがす

説明

<jats:p><jats:bold><jats:italic>Objective—</jats:italic></jats:bold>To determine the role of CXCR2, the receptor for cysteine-X-cysteine (CXC) chemokines, and its primary effector cell, the neutrophil (PMN), on deep venous thrombosis (DVT) resolution.</jats:p><jats:p><jats:bold><jats:italic>Methods and Results—</jats:italic></jats:bold>DVT in BALB/c, anti-CXCR2 antibody-treated, and BALB/c CXCR2<jats:sup>−/−</jats:sup>mice were created by infrarenal inferior vena cava (IVC) ligation and the thrombus harvested at various time points over 21 days. The CXCR2<jats:sup>−/−</jats:sup>mice had significantly larger thrombi at early time points (days 2 to 8), and significantly decreased intrathrombus PMNs, monocytes, and neovascularization as compared with controls. Thrombus KC/CXCL1 was significantly higher at 2 days in CXCR2<jats:sup>−/−</jats:sup>thrombi as measured by enzyme-linked immunosorbent assay. Fibrin content was significantly higher, with less uPA gene expression at 4 days in CXCR2<jats:sup>−/−</jats:sup>thrombi. Late fibrotic maturation of the thrombus was delayed in the CXCR2<jats:sup>−/−</jats:sup>mice, with significantly decreased 8 day MMP-2 activity, whereas MMP-9 activity was elevated as compared with controls. Similar impairment in DVT resolution was found at 8 days with anti-CXCR2 inhibition. However, systemic neutropenia, unlike CXCR2 deletion, did not increase the thrombus size as compared with controls.</jats:p><jats:p><jats:bold><jats:italic>Conclusions—</jats:italic></jats:bold>Normal DVT resolution involves CXCR2-mediated neovascularization, collagen turnover, and fibrinolysis, and it is probably primarily monocyte-dependent.</jats:p>

収録刊行物

被引用文献 (6)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ