EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival



Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival



Transplant International 18(9): 1079-1089



Inhibition or destruction of Kupffer cells (KC) may protect against ischemia-reperfusion (IR) induced primary graft nonfunction (PNF) in liver transplantation. Besides KC activation, PNF is characterized by microvascular perfusion failure, intrahepatic leukocyte accumulation, cell death and hepatocellular dysfunction. KCs can be inactivated by different agents including gadolinium chloride (GdCl3), methyl palmitate (MP) and glycine. The effects of three KC inactivators on IR-injury after rat liver transplantation were compared in the present study. Lewis liver donors were treated with GdCl3, MP, glycine or saline (control). Liver grafts were transplanted following 24 h storage (UW solution). KC populations and IR damage were assessed by histologic analysis, quantitative real-time polymerase chain reaction (RT-PCR) and intravital microscopy. The number of hepatic ED-1 positive macrophages was diminished after GdCl3 (114.8+/-4.4/mm2 liver tissue) and MP treatment (176.0+/-5.0), versus the glycine (263.9+/-5.5) and control (272.1+/-5.6) groups. All three treatment modalities downregulated phagocytic activity for latex particles, paralleled by reduced microvascular injury (acinar perfusion index, GdCl3: 0.75+/-0.03; MP: 0.83+/-.03; glycine: 0.84+/-0.03; 0.63+/-0.03). Quantitative RT-PCR revealed elevated myeloperoxidase mRNA after glycine versus GdCl3 and MP pretreatment (3.2- and 3.4-fold, P=0.011, respectively), without difference to controls (2.9-fold of glycine). TNFalpha-mRNA was reduced after glycine- (5.2-fold), GdCl3- (19.7-fold), MP-treatment (39.5-fold) compared with controls. However, profound prevention of intrahepatic cell death and liver graft failure was solely achieved with glycine preconditioning. Different than GdCl3 and MP, glycine modulates rather than destroys KCs. Glycine appears to preserve cell viability and to TNFalpha/leukocyte dependent organ regeneration capacity, which is related to increase graft survival following liver transplantation.

(PDF emailed within 0-6 h: $19.90)

Accession: 048366410

Download citation: RISBibTeXText

PMID: 16101730

DOI: 10.1111/j.1432-2277.2005.00185.x



Related references

Effects of Kupffer cell inactivation on graft survival and liver regeneration after partial liver transplantation in rats. Hepatobiliary & Pancreatic Diseases International 14(1): 56-62, 2015

Kupffer cell-dependent reperfusion injury in liver transplantation: new clinically relevant use of glycine. Langenbecks Archiv für Chirurgie. Supplement. Kongressband. Deutsche Gesellschaft für Chirurgie. Kongress 115: 185-190, 1999

Role of Kupffer cell activation in the ischemia-reperfusion injury after liver transplantation in the rat. Clinical & Investigative Medicine 17(4 SUPPL ): B64, 1994

Kupffer cell depletion by gadolinium chloride aggravates liver injury after brain death in rats. Molecular Medicine Reports: -, 2018

Kupffer cell erythrophagocytosis and graft-versus-host hemolysis in liver transplantation. Gastroenterology. 110(6): 1891-1896, 1996

Early changes of graft function, cytokines and superoxide dismutase serum levels after donor liver denervation and Kupffer cell depletion in a rat-to-rat liver transplantation model. Hepatobiliary & Pancreatic Diseases International 8(2): 152-156, 2009

Dual role of Kupffer cell activation and endothelial cell damage in reperfusion injury to livers stored for transplantation surgery. Journal Of Gastroenterology & Hepatology. 10(suppl. 1): S84-S87, 1995

Kupffer cell modulation decreases endothelial cell injury and increases survivorship in a rat liver transplant model. Hepatology 10(4): 623, 1989

Kupffer cells potentiate liver sinusoidal endothelial cell injury in sepsis by ligating programmed cell death ligand-1. Journal of Leukocyte Biology 94(5): 963-970, 2014

Ethanol, acetaldehyde and Kupffer cell function: potential role for Kupffer cells in alcohol induced liver injury. Progress in Clinical and Biological Research 325: 255-265, 1990

Gut bacteria drive Kupffer cell expansion via MAMP-mediated ICAM-1 induction on sinusoidal endothelium and influence preservation-reperfusion injury after orthotopic liver transplantation. American Journal of Pathology 182(1): 180-191, 2013

Platelets promote liver regeneration under conditions of Kupffer cell depletion after hepatectomy in mice. World Journal of Surgery 32(6): 1088-1096, 2008

Kupffer cell depletion by gadolinium chloride enhances liver regeneration after partial hepatectomy in rats. American Journal of Physiology 270(6 Pt 1): G909-G918, 1996

Augmenter of liver regeneration promotes hepatic regeneration depending on the integrity of Kupffer cell in rat small-for-size liver transplantation. Journal of Surgical Research 183(2): 922-928, 2013

T-cell depletion for bone marrow transplantation: effects on graft rejection, graft-versus-host disease, graft-versus-leukemia, and survival. Cancer Treatment and Research 50: 99-111, 1990