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Articles by S. P Dineen
Total Records ( 2 ) for S. P Dineen
  A. L Ramos , R Darabi , N Akbarloo , L Borges , J Catanese , S. P Dineen , R. A Brekken and R. C. R. Perlingeiro
  Rationale:

Several studies demonstrate that hematopoietic tissues are a source of endothelial progenitor cells, which contribute to newly formed blood vessels during tissue repair in adults. However, it is not clear which cell type in these hematopoietic tissues gives rise to endothelial progenitor cells.

Objective:

To identity the origin of endothelial progenitors within the hematopoietic hierarchy and to assess their in vivo revascularization potential.

Methods and Results:

Using a single-cell sorting approach and in vitro multilineage differentiation assays, here we show that individual CD34+CD45+CD133+CD38+ cells from cord blood uniquely have the ability to differentiate into T- and B-lymphoid, myeloid, and endothelial cells. The latter were characterized by the expression of VE-cadherin, KDR, von Willebrand factor, endothelial nitric oxide synthase, the lack of CD45, CD133, and c-fms (colony stimulating factor-1 receptor). Unexpectedly when transplanted into hindlimb ischemic NOD-scid IL2Rnull mice, freshly isolated CD34+CD45+CD133+CD38+ cells maintained their hematopoietic identity and were rarely found to integrate into host blood vessels. Nevertheless, they significantly improved perfusion, most likely through a paracrine mechanism. On the other hand, CD34+CD45+CD133+CD38+ cells differentiated in vitro into endothelial cells were able to form vessels in vivo in both Matrigel plug and hindlimb ischemia transplantation assays.

Conclusions:

These findings indicate that the CD34+CD45+CD133+CD38+ cell fraction contains a common progenitor for the hematopoietic and vascular lineages and may represent a valuable cell source for therapeutic applications.

  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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