patocyte in BDL rats. 17 However, the time course and the Supported by grants of the Swiss National Science Foundation to M. S. (3200mechanism of the accumulation of mitochondrial protein in 046804), J.R. (32-45349.95), and S. K. (31-46792.96), and by a grant from the Wolfermann-Naegeli Stiftung to
Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis
β Scribed by K P Rioux; K A Sharkey; J L Wallace; M G Swain
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 980 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
Mast cells have been shown to play a role in many
Mast cells are granulated immunocytes that are bechronic inflammatory and fibrotic disorders. However, lieved to play a role in fibrotic reactions in a variety of their possible contribution to the pathological changes diseases. Increased numbers of mast cells have been that occur in liver cirrhosis is unknown. To explore this, observed in the vicinity of fibrotic lesions in rheumatoid we examined whether changes in hepatic mast cell numarthritis, 1 inflammatory bowel disease, 2,3 scleroderma, 4 ber and mediator content were associated with fibrotic and fibrotic disorders of the lung. 5 Moreover, mast cellchanges in experimental biliary cirrhosis. Rats were derived mediators are known to promote fibroblast studied 7, 14, or 21 days after bile duct resection (BDR). growth 6 and collagen synthesis, 7 and affect the organi-Hepatic mast cells were identified by histochemical and zation and accumulation of connective tissue eleimmunohistochemical stains. Rat mast cell protease II ments. 8 Recent studies have also shown that mast cells (RMCP-II), a marker of mast cell degranulation, was measured in liver by enzyme-linked immunosorbent are themselves capable of synthesizing components of assay. Hepatic collagen deposition was assessed by Sithe extracellular matrix such as collagen and laminin. 9 rius Red F3BA staining. In day 21 BDR rats, there was
In the normal liver, mast cells are closely associated a one-to twofold increase (P Γ΅ .001) in the number of with the portal tracts, but their precise function is not hepatic mast cells, but this was not observed in day 7 or known. It is reasonable to speculate that, as in other 14 BDR rats. Mild fibrotic changes were noted in BDR tissues, hepatic mast cells may be involved in local imrat livers as early as 7 days after induction of cholestasis. munological responses and maintenance and repair of Significant expansion and organization of fibrous tissue connective tissue. 10 Despite active interest in the role had occurred in day 14 BDR rats which progressed to of mast cells in many chronic inflammatory and fibrotic bridging fibrosis by day 21. Liver RMCP-II levels were disorders, mast cells have received little attention as decreased by 50% (P Γ΅ .05) and mast cell degranulation was apparent as shown by histamine immunostaining. possible participants in pathological processes in the These results suggest that hepatic mast cell hyperplasia liver. In one of the few studies of hepatic mast cells and degranulation occur during prolonged cholestasis that exist, Murata et al. examined postmortem liver in the rat. Although these changes do not correlate with biopsy specimens taken from patients who had died of the onset of hepatic fibrosis, they do occur at a time liver diseases and showed that mast cell hyperplasia during which there is significant deposition and organioccurred in cirrhotic livers. 11 Moreover, in this study, zation extracellular matrix elements. Hepatic mast cells, the number of mast cells seemed to correlate with the by releasing profibrogenic mediators, may contribute to accumulation of collagen and other extracellular mafibrotic changes in biliary cirrhosis. (HEPATOLOGY trix elements in the liver.
π SIMILAR VOLUMES
Energy metabolism is abnormal in patients and experimenta! animals with liver cirrhosis. To help better understand the abnormalities, fuel homeostasis and carnitine metabolism were studied in fed and 24-hr-starved rats with secondary biliary cirrhosis induced by bile duct ligation for 4 wk. Plasma k
The hemodynamic responses to terbutalinea selective p,-adrenoceptor agonistwere studied in conscious normal rats and in conscious rats with secondary biliary cirrhosis. Compared with those of normal rats, dose-response curves in cirrhotic rats indicated significantly decreased reactivity in arterial
In liver cirrhosis, down-regulation of endothelial nitric oxide synthase (eNOS) has been implicated as a cause of increased intrahepatic resistance. We investigated whether Rho-kinase activation is one of the molecular mechanisms involved in defective eNOS signaling in secondary biliary cirrhosis. L
targeting NAP to EC/KC results in improved survival, higher SEE EDITORIAL ON PAGE 1680 efficacy, and sparing of renal function in cirrhotic rats. (HEPA-TOLOGY 1997;26:1553-1559.) Endotoxin is thought to play a major role in cirrhotic liver disease. Cyclo-oxygenase inhibitors were shown to be par-End