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Articles by L. B Rivera
Total Records ( 2 ) for L. B Rivera
  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.

  A Villasenor , Z. V Wang , L. B Rivera , O Ocal , I. W Asterholm , P. E Scherer , R. A Brekken , O Cleaver and T. M. Wilkie
  Alethia Villasenor, Zhao V. Wang, Lee B. Rivera, Ozhan Ocal, Ingrid Wernstedt Asterholm, Philipp E. Scherer, Rolf A. Brekken, Ondine Cleaver, and Thomas M. Wilkie

Diabetes is characterized by the loss, or gradual dysfunction, of insulin-producing pancreatic β-cells. Although β-cells can replicate in younger adults, the available diabetes therapies do not specifically target β-cell regeneration. Novel approaches are needed to discover new therapeutics and to understand the contributions of endocrine progenitors and β-cell regeneration during islet expansion. Here, we show that the regulators of G protein signaling Rgs16 and Rgs8 are expressed in pancreatic progenitor and endocrine cells during development, then extinguished in adults, but reactivated in models of both type 1 and type 2 diabetes. Exendin-4, a glucagon-like peptide 1 (Glp-1)/incretin mimetic that stimulates β-cell expansion, insulin secretion and normalization of blood glucose levels in diabetics, also promoted re-expression of Rgs16::GFP within a few days in pancreatic ductal-associated cells and islet β-cells. These findings show that Rgs16::GFP and Rgs8::GFP are novel and early reporters of G protein-coupled receptor (GPCR)-stimulated β-cell expansion after therapeutic treatment and in diabetes models. Rgs16 and Rgs8 are likely to control aspects of islet progenitor cell activation, differentiation and β-cell expansion in embryos and metabolically stressed adults.

 
 
 
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