In view of the participation of vascular endothelial cells (EC) in a wide range of normal and pathological conditions, phenotypic heterogeneity of EC is an important concept for consideration: different sub-populations of EC may play differing biological roles in normal and patho-physiological states

Antigenic heterogeneity of vascular endothelium.

A large body of evidence produced during decades of research indicates that myocardial injury activates innate immunity. On the one hand, innate immunity both aggravates ischemic injury and impedes...

Role of Lymphocytes in Myocardial Injury, Healing, and Remodeling After Myocardial Infarction

The peripheral nerve allograft : a comprehensive review of regeneration and neuroimmunology

BACKGROUNDCell adhesion molecules (CAMs) have been implicated in cardiac allograft rejection. However, previous studies have used qualitative analysis of immunohistochemical data and did not exclude patients with infection or malignancy.METHODS AND RESULTSWe analyzed 40 endomyocardial biopsy specimens from 25 cardiac transplant patients and 8 specimens from patients undergoing cardiac surgery. Patients with evidence of infection or malignancy were excluded. Specimens were stained with monoclonal antibodies against ICAM-1, E-selectin, VCAM-1, and PECAM-1 (which labels all vessels). ICAM-1 expression was assessed by counting ICAM-1-positive vessels and dividing by the total number of vessels (measured by PECAM staining). Specimens were scored as positive or negative for VCAM-1 and E-selectin. We also determined whether serum-soluble ICAM-1 levels (sICAM) correlated with rejection by evaluating 145 serum specimens from 48 cardiac transplant patients and 8 specimens from patients undergoing diagnostic cardiac...

Differential expression of the cell adhesion molecules ICAM-1, VCAM-1, and E-selectin in normal and posttransplantation myocardium. Cell adhesion molecule expression in human cardiac allografts.

Von Willebrand factor (vWf), a glycoprotein involved in
blood coagulation, is synthesized by endothelial cells.
Increased amounts of vWf in blood plasma or tissue samples are
indicative of damaged endothelium. In the present study, mRNA
expression and localization of vWf were determined in irradiated
rat heart tissue. Sprague-Dawley rats received local heart irradiation with
a single dose of 0, 15, or 20 Gy. Hearts were dissected at
different time points (up to 16 months) after irradiation. In a
second experiment, rats were injected with the radioprotector
amifostine (160 mg/kg, i. p.) 15–20 min before irradiation and
sacrificed after 6 months. Immunohistochemistry was performed
using a polyclonal anti-vWf antibody. Serial sections were
subjected to a general rat endothelial cell immunostaining
(RECA-1) or a collagen staining (picrosirius red). mRNA
expression was determined by using PCR. In control tissue, all endothelial cells lining the lumen
of the endocardium and coronary arteries, but not capillary
endothelial cells, were stained for vWf. 1 month after
irradiation with both 15 and 20 Gy, myocardial capillaries
became immunoreactive. From 3 months onward, staining was
observed also within the extracellular matrix (ECM) of fibrotic
areas. At mRNA level, no changes in vWf could be observed at all
time points after irradiation, suggesting that vWf deposition
was not due to increased biosynthesis of the protein. In
sections of amifostine-treated rat hearts, vWf staining was
increased to a lesser extent. These dose- and time-dependent increases in deposition of
vWf indicate the presence of damaged endothelium in the
irradiated rat heart. These increases in vWf accumulation
precede development of fibrosis in the subendocardial layer and
myocardium of the left ventricles, right ventricles, and
atria.

Increased Deposition of von Willebrand Factor in the Rat Heart after Local Ionizing Irradiation

Identification of antigen presenting cells in normal and transplanted human heart: importance of endothelial cells.

Immunocytochemical analysis of endomyocardial biopsies from cardiac transplant patients has defined changes in expression of antigens, expressed on both the myocardium and endothelium which are characteristic of rejection. Biopsies taken from normal donor heart (prior to transplantation) have been compared with biopsies showing histological signs of rejection. There is induction of MHC class I antigen on the normally negative myocardial plasma membrane and induction of the adhesion molecule ICAM-1 on the intercalating discs. Capillary endothelial cells, which constitutively express Class II DR antigen and ICAM-1 in normal heart show increased of endothelial antigens Pal-E and FVIII-RA during rejection. These results demonstrate perturbation of the endothelial system during rejection and possibly indicate damage to the capillary endothelial cells.

Immunocytochemical markers of activation in cardiac transplant rejection

Interest in the endothelium as a possible initiator or target of the antiallograft response prompted the following study. Immunocytochemical techniques have been used to investigate the expression of the endothelial markers EN4, Pal-E, and FVIII-RA in normal human heart, cardiac biopsies from patients with various cardiac diseases (dilated cardiomyopathy [DCM] and myocarditis [MCO]), and cardiac biopsies from heart-transplant recipients undergoing acute rejection or free of rejection. Quantitative data demonstrated greater preponderance of EN4 cells in normal heart than the other markers. In biopsies showing histologic signs of rejection, there was no difference in the number of EN4 positive cells compared to normal. In contrast, there was found a striking increase in the proportion of cells that are Pal-E positive and a significant increase in the proportion of FVIII-RA positive cells in these biopsies. The patient details provided suggest these results do not reflect vascular damage due to cyclosporine but may well reflect damage caused by the rejection process.

Immunocytochemical changes suggestive of damage to endothelial cells during rejection of human cardiac allografts.

Background. Human T cells proliferate in response to both human umbilical vein endothelial cells (HUVEC) and porcine aortic endothelial cells (PAEC) via the second signals LFA-3/CD2 and B7-2 (CD86), respectively. Previous studies have shown that stimulation of T cells via CD28 or phorbol myristate acetate (PMA) activation is highly resistant to inhibition by cyclosporine A (CsA) and tacrolimus (FK506), as is the response of T cells to phytohemmaglutinin in the presence of endothelial cells. We have investigated the inhibitory effects of CsA and FK506 on the direct response of human CD4 + T cells to HUVEC and PAEC and the effect of adding B7-1 transfectants. Methods. T cell proliferation, interleukin-2 release bioassays and a multiple cytokine bioassay employing the TF-1 cell line were used as indicators of T cell responses to HUVEC and PAEC either in the presence or absence of CsA and FK506. In some experiments, B7-1 transfectants were also added. Results. Proliferative responses and interleukin-2 release were highly sensitive to CsA, the ID 50 being significantly less for HUVEC (6.5 ng/ml) than PAEC (15 ng/ml). The ID 50 of CsA for the mixed lymphocyte response (MLR) was similar to PAEC (18.6 ng/ml), all these values being significantly less than the T cell activation by phytohemmaglutinin (PHA) (227 ng/ml). Addition of B7-1 transfectants significantly increased interleukin-2 production by T cells/HUVEC and resistance to CsA was greatly increased to an ID 50 of > 1000 ng/ml. In contrast, addition of B7-1 transfectants to T cells/PAEC had no effect either on T cell proliferation, IL-2 production, or CsA resistance. Similar results were obtained with FK506. Using the TF-1 cell line, it was determined that cytokines other than IL-2 are released during CD4 + T cell/EC interactions, with similar sensitivity to CsA and FK506. Conclusions. It is concluded that both allogeneic and xenogeneic T cell/endothelial responses should be inhibited by therapeutic levels of CsA in vivo, assuming the absence of trans-stimulation by B7 molecules.

Human T cell responses to human and porcine endothelial cells are highly sensitive to cyclosporin A and FK506 in vitro.

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Identification of antigen presenting cells in normal and transplanted human heart: importance of endothelial cells.

Immunocytochemical markers of activation in cardiac transplant rejection

Immunocytochemical changes suggestive of damage to endothelial cells during rejection of human cardiac allografts.

Human T cell responses to human and porcine endothelial cells are highly sensitive to cyclosporin A and FK506 in vitro.