Upregulation of hyaluronan and its binding receptors in an experimental model of chronic cyclosporine nephropathy

Han, Dong He; Song, Ho Kyung; Lee, So Young; Song, Ji‐Hyun; Piao, Shang Guo; Yoon, Hye Eun; Ghee, Jung Yeon; Yoon, Hyung Ju; Kim, Jin; Yang, Chul Woo

doi:10.1111/j.1440-1797.2009.01167.x

Cited by 16 publications

(10 citation statements)

References 36 publications

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“…Including endothelial cells, leukocytes and metastatic tumor cells, CD44 is also expressed in HSCs and MSCs. CD44 is the principal cell surface receptor for HA, which has been shown to accumulate in the cortex in several kidney diseases, such as I/R injury [21], chronic interstitial nephritis [22] and chronic cyclosporine nephropathy [23]. Accordingly, our data showed that HA deposition was readily detectable in remnant model (5/6 Nx).…”

Section: Discussionsupporting

confidence: 56%

The Role of CD44-Hyaluronic Acid Interaction in Exogenous Mesenchymal Stem Cells Homing to Rat Remnant Kidney

Bian

Zhou

Wang

et al. 2013

Kidney Blood Press Res

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Background/Aims: The aim of our study was to reveal the role of CD44-Hyaluronic acid (HA) in the homing and improving renal function of systemically transplanted MSCs in chronic renal failure. Methods: First, a remnant kidney model was established in rats and the expression of HA was determined using immunohistochemistry (IHC) and western blotting. Next, chemotaxis assay using flow cytometry, and cell migration assay of MSCs were performed in vitro. Then, MSCs were transplanted into rats, thus, sprague-Dawley (SD) rats were randomly divided into sham group, 5/6 nephrectomy (5/6 Nx) group, MSC group and MSC/Anti-CD44 group (n = 8 for all groups). Migration of MSCs to the kidney in these rats was assessed by using cell tracking experiments, and tissue damage was evaluated by morphological analysis using Masson's trichrome staining and periodic acid Schiff staining. Results: HA was significantly observed in 5/6 Nx group, but not in sham group. Meanwhile, HA was discovered induced MSCs migration remarkably (p < 0.05) and anti-CD44 antibody inhibited the migration significantly (p < 0.05) in vitro. In vivo, the GFP-MSCs were observed in MSC group and the cells reduced in MSC/Anti-CD44 groups, especially, in the tubulointerstitium. Conclusion: Our findings reveal that CD44-HA has the potential to induce MSCs homing to injured tissue, while its effect on the ability of MSCs, improving tissue function, is not significant.

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Section: Discussionsupporting

confidence: 56%

The Role of CD44-Hyaluronic Acid Interaction in Exogenous Mesenchymal Stem Cells Homing to Rat Remnant Kidney

Bian

Zhou

Wang

et al. 2013

Kidney Blood Press Res

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“…15 A pathogenic role of HA has also been suggested in CKD. For instance, expression of the HA-CD44 pair is highly increased in chronic cyclosporine A-induced nephropathy, 16 experimental crescentic glomerulonephritis, 17 and obstructive nephropathy. 18 Therefore, blocking the interaction between HA and CD44 may prevent the development of fibrosis in CKD.…”

mentioning

confidence: 99%

Lack of hyaluronidases exacerbates renal post-ischemic injury, inflammation, and fibrosis

Colombaro

Jadot

Declèves

et al. 2015

Kidney International

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Renal ischemia-reperfusion injury (IRI) is a pathological process that may lead to acute renal failure and chronic dysfunction in renal allografts. During IRI, hyaluronan (HA) accumulates in the kidney, but suppression of HA accumulation during IRI protects the kidney from ischemic insults. Here we tested whether Hyal1-/- and Hyal2-/- mice display exacerbated renal damage following unilateral IRI due to a higher HA accumulation in the post-ischemic kidney compared with that in the kidney of wild-type mice. Two days after IRI in male mice there was accumulation of HA and CD44 in the kidney, marked tubular damage, infiltration, and increase creatininemia in wild-type mice. Knockout mice exhibited higher amounts of HA and higher creatininemia. Seven days after injury, wild-type mice had a significant decrease in renal damage, but knockout mice still displayed exacerbated inflammation. HA and CD44 together with α-smooth muscle actin and collagen types I and III expression were increased in knockout compared with wild-type mice 30 days after IRI. Thus, both HA-degrading enzymes seem to be protective against IRI most likely by reducing HA accumulation in the post-ischemic kidney and decreasing the inflammatory processes. Deficiency in either HYAL1 or HYAL2 leads to enhanced HA accumulation in the post-ischemic kidney and consequently worsened inflammatory response, increased tubular damage, and fibrosis.

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“…experimental glomerulonephritis [11] and cyclosporin nephropathy [24]. In the current model of AAN both CD44 and HA are strongly linked to fibrotic islets.…”

Section: Discussionmentioning

confidence: 99%

CD44-Positive Cells and Hyaluronan are a Hallmark of a Rat Model of Aristolochic Acid Nephropathy

et al. 2013

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Background: Aristolochic acid (AA) Nephropathy (AAN) is characterized by tubulointerstitial injury leading to fibrosis and tubular atrophy. Defective regeneration of tubular cells was hypothesized as a mechanism leading to Proximal Tubular Epithelial Cell (PTEC) atrophy. Here, we examined the distribution of CD44, an adhesion molecule involved in differentiation, and its main ligand, Hyaluronan (HA), in an experimental AAN model.

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Upregulation of hyaluronan and its binding receptors in an experimental model of chronic cyclosporine nephropathy

Abstract: These findings suggest that upregulation of HA and its binding receptors are involved in interstitial fibrosis in chronic CsA-induced renal injury.

Cited by 16 publications

References 36 publications

The Role of CD44-Hyaluronic Acid Interaction in Exogenous Mesenchymal Stem Cells Homing to Rat Remnant Kidney

The Role of CD44-Hyaluronic Acid Interaction in Exogenous Mesenchymal Stem Cells Homing to Rat Remnant Kidney

Lack of hyaluronidases exacerbates renal post-ischemic injury, inflammation, and fibrosis

CD44-Positive Cells and Hyaluronan are a Hallmark of a Rat Model of Aristolochic Acid Nephropathy

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