scholarly journals Effects of Hyaluronic Acid on Calcium Oxalate Crystallization, Growth, Aggregation, Adhesion on Renal Tubular Cells, and Invasion Through Extracellular Matrix

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 13-13
Author(s):  
Chanettee Chanthick ◽  
Visith Thongboonkerd
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Crystal Growth ◽  
Calcium Oxalate ◽  
Kidney Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Stone Formation

Abstract Objectives Hyaluronic acid (HA), a large non-sulfated glycosaminoglycan, is one of the major components of extracellular matrix (ECM) in connective tissues and other organs. Currently, it is widely used as a dietary supplement, especially for treatment or prevention of aging-related disorders. On the other hand, HA has been reported with an increased risk of kidney stone disease, particularly calcium oxalate (CaOx) type, but with unclear mechanisms. We therefore performed systematic analyses for its modulatory effects on CaOx monohydrate (COM) crystal at various steps of kidney stone formation processes. Methods HA at 1, 10, 100, 1000 and 10,000 ng/ml was tested in various assays for COM crystallization, crystal growth, aggregation, crystal-cell adhesion and invasion through ECM. Results COM crystallization and crystal aggregation were not affected by HA at all concentrations. However, HA significantly promoted COM crystal growth and adhesion onto renal tubular cells in a dose-dependent manner. Interestingly, COM crystal invasion through the ECM was dramatically enhanced by HA even at very low concentration (such as 1 ng/ml). Conclusions Our findings provide evidence for promoting effects of HA on COM crystal growth, adhesion on renal tubular cell surface and invasion through the ECM, all of which are the important steps for kidney stone formation. Funding Sources TRF-IRN grant.

MP33-15 MITOCHONDRIAL COLLAPSE DEPENDS ON CYCLOPHILIN D IN RENAL TUBULAR CELLS PROMOTES KIDNEY STONE FORMATION

2015 ◽  
Vol 193 (4S) ◽  
Author(s):  
Yasuhiko Ito ◽  
Takahiro Yasui ◽  
Kazuhiro Niimi ◽  
Shoichiro Iwatsuki ◽  
Takashi Hamakawa ◽  
...  
Keyword(s):  
Kidney Stone ◽  
Stone Formation ◽  
Cyclophilin D ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Stone Formation

scholarly journals Multicolor imaging of calcium-binding proteins in human kidney stones for elucidating the effects of proteins on crystal growth

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yutaro Tanaka ◽  
Mihoko Maruyama ◽  
Atsushi Okada ◽  
Yoshihiro Furukawa ◽  
Koichi Momma ◽  
...  
Keyword(s):  
Crystal Growth ◽  
Calcium Oxalate ◽  
Kidney Stones ◽  
Calcium Binding ◽  
Kidney Stone ◽  
Stone Formation ◽  
Human Kidney ◽  
In Vivo Effects ◽  
Kidney Stone Formation

AbstractThe pathogenesis of kidney stone formation includes multi-step processes involving complex interactions between mineral components and protein matrix. Calcium-binding proteins in kidney stones have great influences on the stone formation. The spatial distributions of these proteins in kidney stones are essential for evaluating the in vivo effects of proteins on the stone formation, although the actual distribution of these proteins is still unclear. We reveal micro-scale distributions of three different proteins, namely osteopontin (OPN), renal prothrombin fragment 1 (RPTF-1), and calgranulin A (Cal-A), in human kidney stones retaining original mineral phases and textures: calcium oxalate monohydrate (COM) and calcium oxalate dihydrate (COD). OPN and RPTF-1 were distributed inside of both COM and COD crystals, whereas Cal-A was distributed outside of crystals. OPN and RPTF-1 showed homogeneous distributions in COM crystals with mosaic texture, and periodically distributions parallel to specific crystal faces in COD crystals. The unique distributions of these proteins enable us to interpret the different in vivo effects of each protein on CaOx crystal growth based on their physico-chemical properties and the complex physical environment changes of each protein. This method will further allow us to elucidate in vivo effects of different proteins on kidney stone formation.

scholarly journals Losartan Ameliorates Calcium Oxalate-Induced Elevation of Stone-Related Proteins in Renal Tubular Cells by Inhibiting NADPH Oxidase and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Baolong Qin ◽  
Qing Wang ◽  
Yuchao Lu ◽  
Cong Li ◽  
Henglong Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Ang Ii ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Related Proteins ◽  
And Oxidative Stress

Calcium oxalate (CaOx) is the most common type of urinary stone. Increase of ROS and NADPH oxidase gives rise to inflammation and injury of renal tubular cells, which promotes CaOx stone formation. Recent studies have revealed that the renin-angiotensin system might play a role in kidney crystallization and ROS production. Here, we investigated the involvement of Ang II/AT1R and losartan in CaOx stone formation. NRK-52E cells were incubated with CaOx crystals, and glyoxylic acid-induced hyperoxaluric rats were treated with losartan. Oxidative stress statuses were evaluated by detection of ROS, oxidative products (8-OHdG and MDA), and antioxidant enzymes (SOD and CAT). Expression of NADPH oxidase subunits (Nox2 and Nox4), NF-κB pathway subunits (p50 and p65), and stone-related proteins such as OPN, CD44, and MCP-1 was determined by Western blotting. The results revealed upregulation of Ang II/AT1R by CaOx treatment. CaOx-induced ROS and stone-related protein upregulation were mediated by the Ang II/AT1R signaling pathway. Losartan ameliorated renal tubular cell expression of stone-related proteins and renal crystallization by inhibiting NADPH oxidase and oxidative stress. We conclude that losartan might be a promising preventive and therapeutic candidate for hyperoxaluria nephrolithiasis.

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