Volume 62, Issue 5, Pages (November 2002)

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Volume 62, Issue 5, Pages 1560-1569 (November 2002) Multiorgan mRNA misexpression in murine autosomal recessive polycystic kidney disease  Vincent H. Gattone, Justin L. Ricker, Chad M. Trambaugh, Robert M. Klein  Kidney International  Volume 62, Issue 5, Pages 1560-1569 (November 2002) DOI: 10.1046/j.1523-1755.2002.00632.x Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 1 Multiorgan pathology. Cystic pathology in BALB/c-cpk/cpk mice. Grossly (a), common bile duct (arrow) dilation is evident in cystic mouse on right. Note the enlarged cystic kidneys in this 15-day-old cpk/cpk mouse (arrow). The cystic pathology is evident in (b) kidney, (c) liver and (d) pancreas of BALB/c-cpk/cpk mice. Kidney International 2002 62, 1560-1569DOI: (10.1046/j.1523-1755.2002.00632.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 2 mRNA expression in kidney, liver and pancreas. Renal, hepatic and pancreatic mRNA expression from normal and cystic BALB/c-cpk mice by Northern blot hybridization. The expression of c-myc, EGF-R, PKD-1 and histone H4 were elevated in cystic organs. Renal EGF mRNA was severely diminished, while EGF-R mRNA was increased twofold in cystic kidney. The elevated SGP-2 suggests a continued immaturity of the renal collecting duct. Methylene blue staining of 28S and 18S rRNA is shown as a control for RNA loading. N = normal, C = cystic. Kidney International 2002 62, 1560-1569DOI: (10.1046/j.1523-1755.2002.00632.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 3 Cyclin mRNA expression. Renal, hepatic and pancreatic mRNA expression of cyclin genes from normal and cystic BALB/c-cpk mice by ribonuclease protection assay. Compared to normal kidney, cyclin A2, B1 and D2 mRNA expression was increased in cystic kidney while cyclin C and D1 were elevated in the cystic pancreas. None of the cyclin mRNAs were lower in the cystic kidney, cyclin A1, B1 and D2 were lower in the cystic pancreas and cyclin A2, B1, C and D2 were lower in the cystic liver. The cystic biliary duct cells of liver represent a relatively small percentage of the cells in liver; therefore, it is unclear exactly which cell population is responsible for these mRNA data. However, PCNA staining was most prominent in cells lining the intrahepatic biliary cysts. L32 and GAPDH mRNAs are shown as controls. N = normal, C= cystic. Kidney International 2002 62, 1560-1569DOI: (10.1046/j.1523-1755.2002.00632.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 4 bax/bcl-2 family mRNA expression. Renal, hepatic and pancreatic mRNA expression of apoptosis-associated genes from normal and cystic BALB/c-cpk mice by ribonuclease protection assay. Compared to normal kidney, bak, bax, bcl-2 and bad message levels were elevated in cystic kidney and bcl-2 was reduced in liver, while bcl-X mRNA expression was unchanged in cystic kidney and liver. Bcl-x, bak, bax, bcl-2 and bad mRNA levels all were elevated in the cystic pancreas. L32 and GAPDH mRNAs are shown as controls. N = normal, C = cystic. Kidney International 2002 62, 1560-1569DOI: (10.1046/j.1523-1755.2002.00632.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 5 Immunolocalization of c-Myc and PCNA. Immunolocalization of c-Myc and PCNA protein in kidney, liver and pancreas of BALB/c-cpk/cpk mice. PCNA staining is localized to the nuclei of cyst lining epithelial cells in (a) kidney, (b) liver and (c) pancreas of cystic mice. C-Myc staining was evident in nuclei of cells lining renal (d), liver (e) and pancreas (f) cysts. Nuclear PCNA and c-Myc staining was also observed in (a and d) renal epithelial cells lining non-cystic tubules. As a positive control, PCNA and c-Myc staining were particularly prominent in nuclei of cells in the crypts of the intestine (data not shown). (Magnification: a-c, ×250; d-f, ×500) Kidney International 2002 62, 1560-1569DOI: (10.1046/j.1523-1755.2002.00632.x) Copyright © 2002 International Society of Nephrology Terms and Conditions