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Articles by S. A Arnold
Total Records ( 2 ) for S. A Arnold
  S Han , S. A Arnold , S. D Sithu , E. T Mahoney , J. T Geralds , P Tran , R. L Benton , M. A Maddie , S. E D'Souza , S. R Whittemore and T. Hagg
 

Blood vessel loss and inflammation cause secondary degeneration following spinal cord injury. Angiopoietin-1 through the Tie2 receptor, and other ligands through vβ3 integrin, promote endothelial cell survival during developmental or tumour angiogenesis. Here, daily intravenous injections with an vβ3-binding peptide named C16 or an angiopoietin-1 mimetic following a spinal cord contusion at thoracic level 9 in mice rescued epicentre blood vessels, white matter and locomotor function, and reduced detrimental inflammation. Preserved vascularity and reduced inflammation correlated with improved outcomes. C16 and angiopoietin-1 reduced leukocyte transmigration in vitro. Growth factor receptors and integrins facilitate each others’ function. Therefore, angiopoietin-1 and C16 were combined and the effects were additive, resulting in almost complete functional recovery. The treatment had lasting effects when started 4 h following injury and terminated after one week. These results identify vβ3 integrin and the endothelial-selective angiopoietin-1 as vascular and inflammatory regulators that can be targeted in a clinically relevant manner for neuroprotection after central nervous system trauma.

  S. A Arnold , L. B Rivera , A. F Miller , J. G Carbon , S. P Dineen , Y Xie , D. H Castrillon , E. H Sage , P Puolakkainen , A. D Bradshaw and R. A. Brekken
  Shanna A. Arnold, Lee B. Rivera, Andrew F. Miller, Juliet G. Carbon, Sean P. Dineen, Yang Xie, Diego H. Castrillon, E. Helene Sage, Pauli Puolakkainen, Amy D. Bradshaw, and Rolf A. Brekken

Utilizing subcutaneous tumor models, we previously validated SPARC (secreted protein acidic and rich in cysteine) as a key component of the stromal response, where it regulated tumor size, angiogenesis and extracellular matrix deposition. In the present study, we demonstrate that pancreatic tumors grown orthotopically in Sparc-null (Sparc–/–) mice are more metastatic than tumors grown in wild-type (Sparc+/+) littermates. Tumors grown in Sparc–/– mice display reduced deposition of fibrillar collagens I and III, basement membrane collagen IV and the collagen-associated proteoglycan decorin. In addition, microvessel density and pericyte recruitment are reduced in tumors grown in the absence of host SPARC. However, tumors from Sparc–/– mice display increased permeability and perfusion, and a subsequent decrease in hypoxia. Finally, we found that tumors grown in the absence of host SPARC exhibit an increase in alternatively activated macrophages. These results suggest that increased tumor burden in the absence of host SPARC is a consequence of reduced collagen deposition, a disrupted vascular basement membrane, enhanced vascular function and an immune-tolerant, pro-metastatic microenvironment.

 
 
 
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