Chronic Rejection in Experimental Cardiac Transplantation: Studies in the Lewis-F344 Model

1993 ◽  
Vol 134 (1) ◽  
pp. 5-19 ◽  
Author(s):  
David H. Adams ◽  
Mary E. Russell ◽  
Wayne W. Hancock ◽  
Mohamed H. Sayegh ◽  
Lauri R. Wyner ◽  
...  
Keyword(s):  
Chronic Rejection ◽  
Cardiac Transplantation

scholarly journals RhoA- and Actin-Dependent Functions of Macrophages from the Rodent Cardiac Transplantation Model Perspective -Timing Is the Essence

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 70
Author(s):  
Malgorzata Kloc ◽  
Ahmed Uosef ◽  
Martha Villagran ◽  
Robert Zdanowski ◽  
Jacek Z. Kubiak ◽  
...  
Keyword(s):  
Immune Response ◽  
Circadian Rhythm ◽  
Immune Cells ◽  
Chronic Rejection ◽  
Cardiac Transplantation ◽  
Small Gtpase ◽  
Eukaryotic Cells ◽  
Transplantation Model

The small GTPase RhoA, and its down-stream effector ROCK kinase, and the interacting Rac1 and mTORC2 pathways, are the principal regulators of the actin cytoskeleton and actin-related functions in all eukaryotic cells, including the immune cells. As such, they also regulate the phenotypes and functions of macrophages in the immune response and beyond. Here, we review the results of our and other’s studies on the role of the actin and RhoA pathway in shaping the macrophage functions in general and macrophage immune response during the development of chronic (long term) rejection of allografts in the rodent cardiac transplantation model. We focus on the importance of timing of the macrophage functions in chronic rejection and how the circadian rhythm may affect the anti-chronic rejection therapies.

scholarly journals LATE BLOCKADE OF B7-1 COSTIMULATION INTERRUPTS THE DEVELOPMENT OF CHRONIC REJECTION IN A RAT MODEL OF CARDIAC TRANSPLANTATION

1998 ◽  
Vol 65 (12) ◽  
pp. S182
Author(s):  
M D. Denton ◽  
A. Knoflach ◽  
R. Milord ◽  
A. Chandraker ◽  
L. A. Turka ◽  
...  
Keyword(s):  
Rat Model ◽  
Chronic Rejection ◽  
Cardiac Transplantation

scholarly journals Cold ischemia contributes to the development of chronic rejection and mitochondrial injury after cardiac transplantation

2010 ◽  
Vol 23 (12) ◽  
pp. 1282-1292 ◽  
Author(s):  
Stefan Schneeberger ◽  
Albert Amberger ◽  
Julia Mandl ◽  
Theresa Hautz ◽  
Oliver Renz ◽  
...  
Keyword(s):  
Chronic Rejection ◽  
Cardiac Transplantation ◽  
Cold Ischemia ◽  
Mitochondrial Injury

VLA 4, A β1 INTEGRIN, IS ESSENTIAL IN THE PATHOGENESIS OF CHRONIC REJECTION AFTER EXPERIMENTAL CARDIAC TRANSPLANTATION IN RATS.

2000 ◽  
Vol 69 (Supplement) ◽  
pp. S190
Author(s):  
Markus Richter ◽  
Isabel Waligura ◽  
Volkmar Wehner ◽  
Andrea Tannapfel ◽  
Volkmar Falk ◽  
...  
Keyword(s):  
Chronic Rejection ◽  
Cardiac Transplantation ◽  
Β1 Integrin

Immunosuppressive Drugs in Heart Transplantation

2019 ◽  
pp. 83-147
Author(s):  
Sule Apikoglu-Rabus ◽  
Murat B. Rabus ◽  
Rashida Muhammad Umar
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Heart Disease ◽  
Adverse Effects ◽  
Heart Transplantation ◽  
Chronic Rejection ◽  
Cardiac Transplantation ◽  
Immunosuppressive Drugs ◽  
Life Threatening ◽  
End Stage

Congestive heart failure affects 23 million people worldwide [1]. Cardiac transplantation provides a lifesaving treatment for patients with end-stage heart disease. It offers a longer life with a higher quality to those who have no other treatment alternative. Although cardiac transplantation offers a relief from heart immunosuppression. The goal of immunosuppression immediately following surgery is to prevent hyperacute and acute rejections. Transplantation immunosuppression must be balanced in order to prevent rejection while minimizing the serious adverse effects of therapy including life-threatening infections and malignancies. Immunosuppressive regimens are classified as induction, maintenance, or anti-rejection regimens. Induction regimens consist of intense early post-operative immunosuppression while maintenance regimens are used indefinitely for prevention of acute and chronic rejection. This chapter will review the induction and maintenance immunosuppressive regimens used in heart transplantation with summaries of selected literature as well as the most common complications of these therapies and significant drug-drug interactions.

Abstract 377: The Role of Impaired Lymphatic Drainage in Cardiac Transplantation

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Sydney C Ginn ◽  
Lanfang Wang ◽  
Rebecca D Levit
Keyword(s):  
Chronic Rejection ◽  
Cardiac Transplantation ◽  
Transplant Rejection ◽  
Lymphatic Drainage ◽  
Tissue Fluid ◽  
Lymphatic Vasculature ◽  
Lymphatic Development ◽  
Cardiac Allografts ◽  
Pro Inflammatory Cytokines

Functional lymphatic drainage inherently modulates cardiac function by maintaining the immune response and tissue-fluid homeostasis. During cardiac transplantation, the lymphatic collecting vessels are severed at the time of heart excision and not surgically reconstructed in the recipient. The consequence resulting from impaired lymphatic drainage in transplanted hearts is unknown. We hypothesize disruption of lymphatic drainage potentiates chronic inflammation by impeding the egress of immune cells and pro-inflammatory cytokines out of the myocardium exacerbating transplant rejection. Methods: Banked human allograft biopsies were utilized to retrospectively evaluate lymphatic differences between patients that did and did not develop chronic transplant rejection from 1 week to 5 years after surgery. Immunofluorescence staining permitted quantification of normalized lymphatic vessel number and area throughout the lifespan of each cardiac allograft (n=24). Autopsy patients with non-cardiac related fatalities served as controls to delineate normal cardiac lymphatic distribution (n=6). Results: Patients without chronic rejection displayed an initial presence of lymphatic vasculature that steadily declined (n=12), while patients with chronic rejection exhibited a delayed increase in lymphatic development (n=12). Conclusions: These data show significant differences in lymphatic area between patients with and without chronic transplant rejection at critical timepoints, suggesting delayed lymphangiogenesis may correlate with rejection. Translational Impact: These preliminary human data support further investigation into lymphatic-modifying therapeutics to prolong the life of cardiac allografts.

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