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Figure 2 | Fibrogenesis & Tissue Repair

Figure 2

From: HDAC inhibitors in experimental liver and kidney fibrosis

Figure 2

Multidisciplinary techniques for characterization of CCl 4 -induced liver fibrosis and ADR-induced renal fibrosis. Although the liver and kidneys are very distinct organs, common techniques are available for detection of fibrotic damage in them. The top panel shows schemes of the functional units of the kidneys and liver, respectively the glomerulus and the hepatic lobule. Histological staining, Periodic Acid Schiff (PAS) or hematoxylin staining can be performed to study histological changes and are frequently combined with a Sirius Red staining to quantify the degree of matrix deposition or scar formation. Finally, QPCR analysis can provide further information on changes in gene expression upon organ fibrosis. Well-known markers are collagen 1 and alpha-smooth muscle actin, both representing the presence of matrix-producing myofibroblasts. CCl4-induced liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (50 μg/100 g body weight) twice a week for four weeks in BalbC male mice. ADR-induced renal fibrosis was induced by a single intravenous injection of adriamycin (10 mg/kg body weight) and female mice were sacrificed 23 days after ADR injection. The study protocol was approved by the Institutional Animal Care and Use Committee of Vrije Universiteit Brussel, permit numbers 10-212-3 and 09-217-1 and National Institutes of Health principles of laboratory animal care (NIH publication 86–23, revised 1995) were followed. AA, afferent arteriole; CL, capillary loop; CV, central vein; EA, efferent arteriole; HA, hepatic artery; HEP, hepatocyte or hepatocytes; HPV, hepatic portal vein; HSC, hepatic stellate cell; M, mesangial cell; MD, macula densa; P, podocyte.

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