Effect of low-molecular-weight heparin on the commitment of bone marrow cells to liver sinusoidal endothelial cells in CCl4-induced liver injury

2006 ◽  
Vol 34 (4) ◽  
pp. 207-213 ◽  
Author(s):  
N SERIZAWA ◽  
Y TAKEI ◽  
H OKUBO ◽  
S YAMASINA ◽  
N ENOMOTO ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Liver Injury ◽  
Low Molecular Weight Heparin ◽  
Bone Marrow Cells ◽  
Low Molecular Weight ◽  
Liver Sinusoidal Endothelial Cells ◽  
Sinusoidal Endothelial Cells ◽  
Marrow Cells

scholarly journals Structure of a porcine spleen low-molecular-weight inhibitor of in vitro colony formation by bone marrow cells.

1986 ◽  
Vol 34 (5) ◽  
pp. 2251-2253
Author(s):  
YUKITOSHI HAYASE ◽  
YOSIO KANAIWA ◽  
MIHO MURAKAMI ◽  
YOSHINARI TAKAGI ◽  
TAKASHI AMIYA
Keyword(s):  
Molecular Weight ◽  
Bone Marrow ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Low Molecular Weight ◽  
Marrow Cells

scholarly journals Enoxaparin-Induced Liver Injury

2020 ◽  
Vol 14 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Shehriyar Mehershahi ◽  
Nikhitha Mantri ◽  
Aneesh Kumar ◽  
Shaikh Danial ◽  
Patel Harish
Keyword(s):  
Molecular Weight ◽  
Pulmonary Embolism ◽  
Liver Injury ◽  
Low Molecular Weight Heparin ◽  
Liver Enzymes ◽  
Low Molecular Weight ◽  
Dramatic Improvement ◽  
Hepatocellular Injury

Enoxaparin, a form of low-molecular-weight heparin, can cause a rare, underreported, and often reversible form of hepatocellular injury. This report describes a case of enoxaparin-induced hepatotoxicity in a 61-year-old male diagnosed with pulmonary embolism. Elevations of liver enzymes were noted within 1 week of starting the drug, followed by a dramatic improvement upon its discontinuation, with subsequent normalization in the following days.

HEPARIN STIMULATES FIBROBLAST GROWTH INDUCED BY PDGF

1987 ◽  
Author(s):  
E Dupuy ◽  
P S Rohrlich ◽  
G Tobelem
Keyword(s):  
Molecular Weight ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Muscle Cells ◽  
Low Molecular Weight ◽  
Thymidine Uptake ◽  
Fibroblast Proliferation

Heparin binds to smooth muscle cells and endothelial cells. It inhibits the proliferation of the smooth muscle cells and modulates the growth of endothelial cells. Fibroblasts which represent an other cell type belonging to the vascular wall could also have their growth modified by heparin. We have at first, demonstrated that 125I unfractionated heparin bigds to cultured human skin fibroblasts with a Kd of 1.16 10 M.A low molecular weight heparin fraction (PK 10169) competed (50 %)with I unfractionated heparin, but at aless extent than cold unfractionated heparin(90%).As it has been reported with endothelial and smooth muscle cells, about 30% of the bound unfractionated heparin was internalized bythe fibroblasts. Heparin alone at the concentration ranges from 0 to 10-5M has no effect on fibroblast proliferation measured by the H thymidine uptake. When the cellproliferation was induced by pure PDGF, heparin potentiated markedly the fibroblast growth.The effgct started at 10-8 M heparinand reached a plateau from 10-6 M to 10-5 M. Similar stimulationwas observed when the growth was induced by FGF or EGF. Low molecular weight heparin enhanced the fibroblast proliferation induced by PDGF but at a less extent than unfractionated heparin, chondroltin sulfate has no effect. When added during the cell culture growth withhuman serum (5%), unfractionated heparin increased by 48 the cell proliferation as measured bycell counting at the 6th day of the culture. PDGF did not modify the heparin binding on fibroblast cultures either at 4°C or 37°C and did not alter the process of heparin internalization. JDGF binding to the cultured fibroblast (Kd 10.1 ± 3.4 10-10 M)was not modified by the presence of heparin when studied at 4°C.In conclusion : i) cultured human fibroblasts bind and internalize heparin, ii) heparinand heparin fraction stimulate the fibroblastgrowth induced by PDGF, iii) since the binding of PDGF is not modified by bound heparin, the mechanism of stimulation remains unknown.

scholarly journals Evidence of the existence of a factor that induces Fc receptors on bone marrow cells

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 756-760 ◽  
Author(s):  
M Calcagno ◽  
JR Perez ◽  
MG Waldo ◽  
G Cabrera ◽  
B Weiss-Steider
Keyword(s):  
Molecular Weight ◽  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Colony Stimulating Factor ◽  
Isoelectric Ph ◽  
Bacterial Lipopolysaccharides ◽  
Molecular Sieving ◽  
Stimulating Factor ◽  
Density Gradient Sedimentation ◽  
Marrow Cells

Abstract The existence of a molecule responsible for the induction of Fc receptor (FcR) on bone marrow cells (FcR inducer, FcRI) is demonstrated in conditioned media from the macrophage-like cell line WR19M.1 activated by bacterial lipopolysaccharides. The molecular weight obtained from molecular sieving chromatography in gel and density gradient sedimentation is found to be 18,500 daltons and 16,000 daltons, respectively, with an isoelectric pH of 7.4. The factor is found to be thermolabile and trypsin sensitive. The macrophage and granulocyte inducer (MGI), also known as colony-stimulating factor (CSF) or colony-stimulating activity (CSA), is identified from the same source and found to have a molecular weight and an isoelectric pH different from FcRI. The fractions that contained the MGI did not induce FcR on bone marrow cells, while the fractions rich in FcRI did not induce colony formation.

Expression of P-Selectin on Hepatic Endothelia and Platelets Promoting Neutrophil Removal by Liver Macrophages

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 520-528
Author(s):  
Jialan Shi ◽  
Yoshihiro Kokubo ◽  
Kenjiro Wake
Keyword(s):  
Molecular Weight ◽  
Endothelial Cells ◽  
Kupffer Cells ◽  
Polymorphonuclear Leukocyte ◽  
Low Molecular Weight Heparin ◽  
Acute Inflammation ◽  
Combined Treatment ◽  
Gadolinium Chloride ◽  
Low Molecular Weight

The role of P-selectin on polymorphonuclear leukocyte (PMN) adhesion-induced PMN elimination in the liver is unclear. Our objectives were to show the expression and distribution of P-selectin in rat liver, as well as to evaluate the changes in the modulation of the expression of P-selectin and its role in the accumulation and sequestration of PMNs. The intravenous administration of endotoxin markedly increased the expression of P-selectin on the venous and sinusoidal endothelial cells, as well as on the platelets trapped in the liver. Its expression peaked at 6 hours postinjection and was associated with a rapid increase in the aggregation and elimination of PMNs in the hepatic sinusoids. Combined treatment with an antibody to P-selectin or with low molecular weight heparin, a P-selectin antagonist, blocked the P-selectin, significantly reduced the arrest of PMNs, and delayed their removal in the liver. Pretreatment with gadolinium chloride inhibited phagocytosis of PMNs by the Kupffer cells, decreased the expression of P-selectin, and limited the hepatic accumulation of PMNs. Thus, P-selectin played a role in accumulation and elimination of PMNs from the liver. Results also suggest that activated Kupffer cells can modulate the expression of P-selectin in the liver and influence the homeostasis of PMNs in the circulation during acute inflammation.

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