Genome‐Wide Transcription Profile of Endothelial Cells After Cardiac Transplantation in the Rat

Abstract

Transcriptome analyses of organ transplants have until now usually focused on whole tissue samples containing activation profiles from different cell populations. Here, we enriched endothelial cells from rat cardiac allografts and isografts, establishing their activation profile at baseline and on days 2, 3 and 4 after transplantation. Modulated transcripts were assigned to three categories based on their regulation profile in allografts and isografts. Categories A and B contained the majority of transcripts and showed similar regulation in both graft types, appearing to represent responses to surgical trauma. By contrast, category C contained transcripts that were partly allograft-specific and to a large extent associated with interferon-cresponsiveness. Several transcripts were verified by immunohistochemical analysis of graft lesions, among them the matricellular protein periostin, which was one of the most highly upregulated transcripts but has not been associated with transplantation previously. In conclusion, the majority of the differentially expressed genes in graft endothelial cells are affected by the transplantation procedure whereas relatively few are associated with allograft rejection.

Increased Expression of Periostin in Vitreous and Fibrovascular Membranes Obtained from Patients with Proliferative Diabetic Retinopathy

“…However, some earlier studies showed that periostin is produced by endothelial cells enriched from cardiac grafts, suggesting that periostin may exhibit tissuespecific pattern of expression. 47 Additionally, periostin was also expressed in myofibroblast-like cells in the stroma of FVMs. It has been reported that a stable expression of a periostin transgene in 293T cells causes the cells to undergo fibroblast-like transformation, and the cells expressing ectopic periostin increased cell migration, invasion, and adhesion.…”

Inflammatory markers sampled by microdialysis catheters distinguish rejection from ischemia in liver grafts

“…A biological explanation for the selective increase in CXCL10 being related to rejection and not ischemia may be the precursor interferon-c, which probably is independent of complement activation. 41,42 The complement system represents the innate immune system, and the biologically highly potent activation product C5a is induced by the activation of all initial activation pathways. C5a has a number of effector functions and is, for example, a powerful chemoattractant causing the accumulation of neutrophil granulocytes and an important inducer of inflammation.…”

Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation

“…Early T-cell reaction precedes alloantigen priming and induces graft necrosis [36, 37]. Inflammatory activation of graft endothelium [38], platelets, the coagulation cascade, and the complement system [39] plays important roles in early graft injury and subsequent graft vasculopathy.…”