TY - JOUR

T1 - Basement membrane chondroitin sulfate proteoglycan alterations in a rat model of polycystic kidney disease.

AU - Ehara, T

AU - Carone, F A

AU - McCarthy, K J

AU - Couchman, J R

N1 - Keywords: Aging; Animals; Basement Membrane; Chondroitin Sulfates; Collagen; Disease Models, Animal; Fibronectins; Fluorescent Antibody Technique; Kidney Tubules; Laminin; Male; Phenols; Polycystic Kidney Diseases; Rats; Rats, Sprague-Dawley; Staining and Labeling

PY - 1994

Y1 - 1994

N2 - Alterations in basement membrane components, notably proteoglycans, in a rat model of polycystic kidney disease have been investigated. Rats were fed phenol II (2-amino-4-hydroxyphenyl-5-phenyl thiazole) for 4 days and then changed to normal diet for a 7-day recovery period. Marked dilation of distal tubules and collecting ducts was observed by 4 days with phenol II treatment, but the morphology returned to normal after 7 days of subsequent normal diet. Staining of tissue sections with two mouse monoclonal antibodies to a recently described basement membrane chondroitin sulfate proteoglycan (BM-CSPG) core protein was markedly diminished in the basement membranes of dilated cystic tubules. Reduction in staining was evident as early as 2 days. During recovery, BM-CSPG increased in tubular basement membranes and returned to normal after 7 days. Staining with a polyclonal antibody to chondroitin sulfate chains confirmed these changes in cystic tubule basement membranes. During the recovery stage, interstitial chondroitin sulfate (representing a CSPG other than BM-CSPG) was greatly increased around these tubules, along with the glycoprotein fibronectin. Staining with antibody to a basement membrane heparan sulfate proteoglycan core protein related to perlecan did not diminish but rather stained affected tubules intensely, whereas laminin, on the other hand, was apparently diminished in the basement membranes of the cystic tubules. Type IV collagen staining did not change through disease onset or recovery. These results suggest that BM-CSPG, which was rapidly altered in distribution through the onset and recovery phases, may be a sensitive marker of the cystic state, and in addition, the expression of basement membrane proteoglycans may be specifically and separately regulated in this disease.

AB - Alterations in basement membrane components, notably proteoglycans, in a rat model of polycystic kidney disease have been investigated. Rats were fed phenol II (2-amino-4-hydroxyphenyl-5-phenyl thiazole) for 4 days and then changed to normal diet for a 7-day recovery period. Marked dilation of distal tubules and collecting ducts was observed by 4 days with phenol II treatment, but the morphology returned to normal after 7 days of subsequent normal diet. Staining of tissue sections with two mouse monoclonal antibodies to a recently described basement membrane chondroitin sulfate proteoglycan (BM-CSPG) core protein was markedly diminished in the basement membranes of dilated cystic tubules. Reduction in staining was evident as early as 2 days. During recovery, BM-CSPG increased in tubular basement membranes and returned to normal after 7 days. Staining with a polyclonal antibody to chondroitin sulfate chains confirmed these changes in cystic tubule basement membranes. During the recovery stage, interstitial chondroitin sulfate (representing a CSPG other than BM-CSPG) was greatly increased around these tubules, along with the glycoprotein fibronectin. Staining with antibody to a basement membrane heparan sulfate proteoglycan core protein related to perlecan did not diminish but rather stained affected tubules intensely, whereas laminin, on the other hand, was apparently diminished in the basement membranes of the cystic tubules. Type IV collagen staining did not change through disease onset or recovery. These results suggest that BM-CSPG, which was rapidly altered in distribution through the onset and recovery phases, may be a sensitive marker of the cystic state, and in addition, the expression of basement membrane proteoglycans may be specifically and separately regulated in this disease.

M3 - Journal article

C2 - 7510458

VL - 144

SP - 612

EP - 621

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 3

ER -