Characterization of microvascular endothelial cells isolated from the dermis of adult mouse tails.

Dermal microvascular endothelial cells (DMECs) play an important role in physiological and pathophysiological processes such as wound healing, cell differentiation, antigen-presentation, inflammation, tumor metastasis, and diabetes. The study of these processes requires a suitable and accessible in vitro model, such as murine DMECs (mDMECs). However, since these cells are difficult to isolate and propagate, some of their properties are not fully characterized.

Flow cytometric isolation and phenotypic characterization of two subsets of ED2(+) (CD163) hepatic macrophages in rats.

Aims: Macrophages in the liver are well known for their functional heterogeneity. However, subpopulations of the hepatic macrophages are not well defined.

Methods: Two subsets of hepatic macrophages isolated from rats via FACS with immunolabeling of ED2 (anti-CD163) antibody were studied for phenotypic and functional characteristics.

Genetic modulation of CD44 expression by intragraft fibroblasts.

This study investigated the genetic composition and the functional implication of CD44 species expressed by intragraft fibroblasts. An LEW-to-F344 heart transplant model of chronic rejection was used. Intragraft fibroblasts recovered from the chronically rejecting allografts displayed a 4.

Anti-CD20 antibody suppresses anti-HLA antibody formation in a HLA-A2 transgenic mouse model of sensitization.

Background: B cell depletion by anti-CD20 antibody is used in desensitization protocols and for treatment of antibody-mediated rejection (AMR). However, little is known about the efficacy and the mechanism(s) of action.

Methods: A mouse model of HLA sensitization was used to study the effectiveness of anti-CD20 treatment on B cell depletion and anti-HLA antibody suppression.

Interaction of CD44 and hyaluronic acid enhances biliary epithelial proliferation in cholestatic livers.

Biliary epithelia express high levels of CD44 in hepatobiliary diseases. The role of CD44-hyaluronic acid interaction in biliary pathology, however, is unclear. A rat model of hepatic cholestasis induced by bile duct ligation was employed for characterization of hepatic CD44 expression and extracellular hyaluronan distribution.

Rat chemokine CXCL11: structure, tissue distribution, function and expression in cardiac transplantation models.

CXCL11 is thought to play a critical role in allograft rejection. To clarify the role of CXCL11 in the rat transplantation model, we cloned CXCL11 cDNA from rat liver tissue and used it to study CXCL11 structure, function and expression. The rat CXCL11 gene encodes a protein of 100 amino acids and spans approximately a 2.

Contribution of mesenchymal progenitor cells to tissue repair in rat cardiac allografts undergoing chronic rejection.

Background: Mesenchymal progenitor cells (MPC) have recently been demonstrated to actively migrate into cardiac allografts during chronic rejection. This study examines the role of MPC in tissue repair of heart allografts in a rat model of chronic rejection.

Methods: The potential of a rat MPC line (Ap8c3) to differentiate to myofibroblasts and cardiomyocytes was studied in differentiation cultures.

The role of the hyaluronan receptor CD44 in mesenchymal stem cell migration in the extracellular matrix.

In a previous investigation, we demonstrated that mesenchymal stem cells (MSCs) actively migrated to cardiac allografts and contributed to graft fibrosis and, to a lesser extent, to myocardial regeneration. The cellular/molecular mechanism responsible for MSC migration, however, is poorly understood. This paper examines the role of CD44-hyaluronan interaction in MSC migration, using a rat MSC line Ap8c3 and mouse CD44-/- or CD44+/+ bone marrow stromal cells (BMSCs).

Identification, functional analysis and expression in a heterotopic heart transplant model of CXCL9 in the rat.

CXCR3 chemokines are of particular interest because of their potential involvement in a variety of inflammatory diseases, including the rejection of organ transplants. Although the rat is one of the most appropriate animals for using to study transplantation biology, the structural and functional characteristics of CXCL9 [monokine induced by interferon-gamma (Mig)] in this experimental model have not been described. Therefore, we recently conducted a series of experiments to identify and characterize the rat CXCL9 gene.

Evidence for recipient derived fibroblast recruitment and activation during the development of chronic cardiac allograft rejection.

Background: Allograft fibrosis is a prominent feature of chronic rejection. Although intragraft fibroblasts contribute to this process, their origin and exact role remain poorly understood.

Methods: Using a rat model of chronic rejection, LEW to F344, cardiac fibroblasts were isolated at the point of rejection and examined in a collagen gel contraction assay to measure fibroblast activation.

Predominant expression of the Th2 response in chronic cardiac allograft rejection.

Chronic rejection is the main cause of late allograft failure in patients. CD4+ T cells activated by indirect recognition of alloantigens are implicated in this rejection reaction. However, the type of T cell response (Th1 vs Th2) that contributes to chronic rejection has not been fully investigated.

Migration of mesenchymal stem cells to heart allografts during chronic rejection.

Background: Mesenchymal stem cells (MSC) are pluripotent progenitors for a variety of cell types, including fibroblasts and muscle cells. Their involvement in the tissue repair of allografts during the development of chronic rejection has been hypothesized, but not yet substantiated, by experimental evidence.

Methods: Rat MSC were isolated from circulation using an aortic pouch allograft as a trapping device.

Vascular endothelial cell apoptosis induced by anti-donor non-MHC antibodies: a possible injury pathway contributing to chronic allograft rejection.

Background: Non-major histocompatibility complex (non-MHC) alloantibodies may play a pathogenic role in chronic rejection but remain poorly characterized.

Methods: The kinetics of alloantibody production and the mechanism by which non-MHC alloantibodies cause graft injury were investigated in a Lewis-to-Fischer 344 (LEW-to-F344) rat model of cardiac transplantation.

Results: Flow cytometry detected that all the F344 recipients of LEW allografts produced anti-donor immunoglobulin G (IgG) antibodies reactive with LEW lymphocytes and endothelial cells.