Role of Heparan Sulfate Proteoglycan(Syndecan-1) on the Renal Epithelial Cells During Calcium Oxalate Monohydrate Crystal Attachment.

Abstract

We have reported that heparan sulfate (HS)/heparan sulfate proteoglycan (HSPG, syndecan-1) expression significantly increased in the rat kidney during calcium oxalate (CaOx) normal conditions. However, calcium oxalate crystal attachment was apparently decreased in the KIC-synd-1 cells. These results suggested that cell surface HS/syndecan-1 has preventive role for calcium oxalate nephrolithiasis via creation of a charge barrier against COM crystal attachment.

Increased Expression of Heparan Sulfate Proteoglycan on the Cultured Renal Epithelial Cells during Oxalate Exposure

“…Unfortunately, previous reports failed to confirm the exact role of cell surface HS, because the wild type MDCK cells do not express any type of cell surface heparan sulfate proteoglycan (HSPG, syndecan) [11]. Recently, we established novel MDCK cell lines (KIC-synd-1) that expressed the human syndecan-1 gene, and we confirmed that cell surface HS inhibited the COM crystal cell attachment [12]. In the present study, we examined the change of heparan sulfate proteoglycan (syndecan-1) expression on the KIC-synd-1 cells during oxalate exposure.…”

“…Newly established MDCK transfectant that expressed human-syndecan-1 (KIC-synd-1) were grown in similar growth media containing neomycin (G418, 20 μg/ml). This cell line was transformed with human syndecan-1 cDNA derived from the human prostate cancer cell line (LNCaP; ATCC CRL 1740, Dainippon Pharmaceutical Co., Osaka, Japan) [12]. KIC-synd-1 cells that we established from MDCK transfectant has already been recognized at our ethical committee.…”

The effects of intracrystalline and surface‐bound proteins on the attachment of calcium oxalate monohydrate crystals to renal cells in undiluted human urine

“…Using such models, it has been shown that phosphotidylserine [1], proteins containing sialic acid [2,3], collagen IV [4], an acidic fragment of nucleolin‐related protein [5], Annexin‐II [6], osteopontin [7,8] and hyaluronan [9] mediate the attachment of calcium oxalate (CaOx) monohydrate (COM) crystals to renal epithelial cells. On the other hand, fibronectin [10], osteopontin [11], bikunin [12], heparan sulphate/syndecan‐1 [13], hepatocyte growth factor [14], Tamm‐Horsfall glycoprotein (THG) [11] chondroitin sulphates A and B [11], heparan sulphate [11], TGFβ 2 [15] and undifferentiated urinary macromolecules [16–18] have been reported to reduce the adhesion of COM crystals. Inhibitory effects of macromolecules have been shown by altering the macromolecular composition of either the incubation medium in which crystal attachment was assessed [10,11,12,15,19] or the surfaces of the renal tubular cells [3,5,6,8,20,21].…”

Characterization of glycosaminoglycans in tubular epithelial cells: Calcium oxalate and oxalate ions effects

“…The increased expression of syndecan-1 and heparan sulfate in a cell line derived from MDCK cells led to a decrease in calcium oxalate attachment to these cells [23], suggesting a preventive role for this proteoglycan in calcium oxalate nephrolithiasis.…”