337 INVESTIGATING THE TISSUE TURNOVER PROFILE IN LIVER FIBROSIS BY NOVEL BIOCHEMICAL MARKERS OF EXTRACELLULAR MATRIX REMODELING

2011 ◽  
Vol 54 ◽  
pp. S135
Author(s):  
D.J. Leeming ◽  
S.S. Veidal ◽  
E. Vassiliadis ◽  
N. Barascuk ◽  
Y. He ◽  
...  







Dose-Response ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. 155932581878983 ◽  
Author(s):  
Cornel Balta ◽  
Alina Ciceu ◽  
Hildegard Herman ◽  
Marcel Rosu ◽  
Oana Maria Boldura ◽  
...  

Liver fibrosis represents an overaccumulation of extracellular matrix (ECM). This study was designed to investigate the effect of chrysin on established ECM overproduction in carbon tetrachloride (CCl4) mouse liver fibrosis. Experimental fibrosis was induced by intraperitoneal injection of 2 mL/kg CCl4 twice a week, for 7 weeks. Mice were orally treated with 3 doses of chrysin (5,7-dihydroxyflavone). For the assessment of the spontaneous reversion of fibrosis, CCl4-treated mice were investigated after 2 weeks of recovery time. Silymarin was used as a standard of liver protection. In fibrotic livers, the results showed the upregulation of collagen I (Col I) and tissue inhibitors of metalloproteinase 1 (TIMP-1) and modulation of matrix metalloproteinases (MMPs), which led to an altered ECM enriched in Col, confirmed as well by electron microscopy investigations. Treatment with chrysin significantly reduced ultrastructural changes, downregulated Col I, and restored TIMP-1/MMP balance, whereas in the group observed for the spontaneous regression of fibrosis, they remained in the same pattern with fibrotic livers. In this study, we have shown chrysin efficacy to attenuate dose-dependent CCl4-stimulated liver ECM accumulation by regulation of MMP/TIMP imbalance and inhibition of Col production. We have shown the dose-dependent chrysin efficiency in attenuation of CCl4-induced liver ECM accumulation by regulation of MMP/TIMP imbalance and inhibition of Col production. Our findings suggest that chrysin oral administration may introduce a new strategy for treating liver fibrosis in humans.



Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1046
Author(s):  
Jorge Martinez ◽  
Patricio C. Smith

Desmoplastic tumors correspond to a unique tissue structure characterized by the abnormal deposition of extracellular matrix. Breast tumors are a typical example of this type of lesion, a property that allows its palpation and early detection. Fibrillar type I collagen is a major component of tumor desmoplasia and its accumulation is causally linked to tumor cell survival and metastasis. For many years, the desmoplastic phenomenon was considered to be a reaction and response of the host tissue against tumor cells and, accordingly, designated as “desmoplastic reaction”. This notion has been challenged in the last decades when desmoplastic tissue was detected in breast tissue in the absence of tumor. This finding suggests that desmoplasia is a preexisting condition that stimulates the development of a malignant phenotype. With this perspective, in the present review, we analyze the role of extracellular matrix remodeling in the development of the desmoplastic response. Importantly, during the discussion, we also analyze the impact of obesity and cell metabolism as critical drivers of tissue remodeling during the development of desmoplasia. New knowledge derived from the dynamic remodeling of the extracellular matrix may lead to novel targets of interest for early diagnosis or therapy in the context of breast tumors.





2006 ◽  
Vol 95 (1) ◽  
pp. 215-226 ◽  
Author(s):  
Eric A. Andreasen ◽  
Lijoy K. Mathew ◽  
Christiane V. Löhr ◽  
Rachelle Hasson ◽  
Robert L. Tanguay


2004 ◽  
Vol 191 (6) ◽  
pp. S10
Author(s):  
Wendy Kinzler ◽  
John Smulian ◽  
C. Andrew Kistler ◽  
Rita Hahn ◽  
Peihong Zhou ◽  
...  


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