Hepatic Stellate Cells
Mostrando 13-24 de 50 artigos, teses e dissertações.
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13. Four whole-istic aspects of schistosome granuloma biology: fractal arrangement, internal regulation, autopoietic component and closure
This paper centers on some whole-istic organizational and functional aspects of hepatic Schistosoma mansoni granuloma, which is an extremely complex system. First, it structurally develops a collagenic topology, originated bidirectionally from an inward and outward assembly of growth units. Inward growth appears to be originated from myofibroblasts derived f
Memórias do Instituto Oswaldo Cruz. Publicado em: 2006-10
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14. Produção de mediadores eosinofílicos pelas células estreladas hepáticas durante a esquitossomose experimental murina. / Production of mediators Eosinophils for covered with stellate cells hepatic during experimental schistosomiasis mansoni.
As células conjuntivas hepáticas possuem um papel importante na patogênese da infecção por Schistosoma mansoni, e dentre essas células destacam-se as células estreladas hepáticas. As células estreladas hepáticas derivadas do granuloma esquistossomótico podem ser cultivadas in vitro, sendo denominadas células GR. No estado fisiológico, essas cél
Publicado em: 2006
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15. On the presence of hepatic stellate cells in portal spaces
Previous studies in mice with hypervitaminosis A have demonstrated that fat-storing cells (hepatic stellate cells-HSCs) participate in schistosomal granuloma fibrogenesis. The origin of such cells in portal areas, away from the Disse spaces, was herein investigated. HSCs were identified in frozen sections of the liver by means of Sudan III staining. They app
Memórias do Instituto Oswaldo Cruz. Publicado em: 2005-05
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16. Expression of the Na+/Ca2+ exchanger emerges in hepatic stellate cells after activation in association with liver fibrosis
Activation of hepatic stellate (Ito) cells is a final common pathway of liver fibrosis. The findings presented in this paper indicate that expression of Na+/Ca2+ exchanger (NCX) emerges in rat hepatic stellate cells after activation in vitro during primary culture or in vivo in response to intoxication with CCl4. NCX mRNA became detectable by Northern blot a
The National Academy of Sciences.
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17. Activation of hepatic stellate cells by TGF alpha and collagen type I is mediated by oxidative stress through c-myb expression.
Excessive production of collagen type I is a major contributor to hepatic fibrosis. Activated (myofibroblastic), but not quiescent, hepatic stellate cells (lipocytes) have a high level of collagen type I and alpha-smooth muscle actin expression. Therefore, stellate cell activation is a critical step in hepatic fibrosis. Here we show that quiescent stellate c
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18. Proliferation of hepatic stellate cells is inhibited by phosphorylation of CREB on serine 133.
Proliferating, activated, hepatic stellate cells have a high level of collagen type I expression. Therefore, stellate cell proliferation is a critical step in hepatic fibrosis. Here we show that proliferation of activated primary rat stellate cells was blocked by elevation of cAMP with 8 Br-cAMP or isomethylbutyl xanthine, a phosphodiesterase inhibitor, and
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19. Endothelin antagonism in experimental hepatic fibrosis. Implications for endothelin in the pathogenesis of wound healing.
The liver's response to chronic injury is fibrosis, which is analogous to wound healing in other organs. Hepatic wounding is characterized by the "activation" of resident stellate cells (lipocytes, Ito cells) to myofibroblast-like cells that produce increased amounts of smooth muscle alpha-actin and extracellular matrix. Stellate cells possess abundant endot
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20. Mac the knife? Macrophages– the double-edged sword of hepatic fibrosis
Progression of hepatic fibrosis requires sustained inflammation leading to activation of stellate cells into a fibrogenic and proliferative cell type, whereas regression is associated with stellate cell apoptosis. The contribution of hepatic macrophages to these events has been largely overlooked. However, a study in this issue of the JCI demonstrates that m
American Society for Clinical Investigation.
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21. Cell and Molecular Regulation of Endothelin-1 Production during Hepatic Wound Healing
During hepatic wound healing, activation of key effectors of the wounding response known as stellate cells leads to a multitude of pathological processes, including increased production of endothelin-1 (ET-1). This latter process has been linked to enhanced expression of endothelin-converting enzyme-1 (ECE-1, the enzyme that converts precursor ET-1 to th
The American Society for Cell Biology.
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22. DDR2 receptor promotes MMP-2–mediated proliferation and invasion by hepatic stellate cells
Type I collagen provokes activation of hepatic stellate cells during liver injury through mechanisms that have been unclear. Here, we tested the role of the discoidin domain tyrosine kinase receptor 2 (DDR2), which signals in response to type I collagen, in this pathway. DDR2 mRNA and protein are induced in stellate cells activated by primary culture or in v
American Society for Clinical Investigation.
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23. Gene transfer of the neuronal NO synthase isoform to cirrhotic rat liver ameliorates portal hypertension
Reduced production of nitric oxide (NO) in the cirrhotic liver results from a defect in hepatic endothelial cell nitric oxide synthase (ecNOS) and appears to contribute to the high intrahepatic resistance and portal hypertension typical of cirrhosis. Therefore, we postulated that targeting a heterologous NOS isoform to sinusoidal endothelial cells or other p
American Society for Clinical Investigation.
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24. In vivo inhibition of rat stellate cell activation by soluble transforming growth factor β type II receptor: A potential new therapy for hepatic fibrosis
Transforming growth factor β (TGF-β) is a well characterized cytokine that appears to play a major role in directing the cellular response to injury, driving fibrogenesis, and, thus, potentially underlying the progression of chronic injury to fibrosis. In this study, we report the use of a novel TGF-β receptor antagonist to block fibrogenesis induced by l
The National Academy of Sciences.