Urinary Periostin Excretion Predicts Renal Outcome in IgA Nephropathy

Hwang, Jin Ho; Lee, Jung Pyo; Kim, Clara Tammy; Yang, Seung Hee; Kim, Jin‐Hyuk; An, Jung Nam; Moon, Kyung Chul; Lee, Hajeong; Oh, Yun Kyu; Joo, Kwon Wook; Kim, Yon Su; Lim, Chun Soo

doi:10.1159/000452228

Cited by 32 publications

(37 citation statements)

References 26 publications

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“…We previously reported that the urine periostin excretion at the time of a renal biopsy correlated with tissue fibrosis and renal outcomes in biopsy-proven IgA nephropathy patients [20]. Fibrotic tissue contains periostin, and it can be secreted in urine and detected in the early stage of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

“…Extensive investigations of this protein have been conducted in various neoplasms, asthma, and cardiac diseases [9-12]. Recently, periostin has emerged as a player in the field of nephrology [13-20]. Periostin is known to be expressed mainly in the tubulointerstitial areas in renal fibrosis, and a relationship between urinary periostin level, tubular damage, autosomal dominant polycystic kidney disease, and chronic allograft nephropathy has been reported [13, 15, 16].…”

Section: Introductionmentioning

confidence: 99%

“…Periostin is known to be expressed mainly in the tubulointerstitial areas in renal fibrosis, and a relationship between urinary periostin level, tubular damage, autosomal dominant polycystic kidney disease, and chronic allograft nephropathy has been reported [13, 15, 16]. Recent research has elucidated the significance of periostin as tissue or urinary biomarker in type 2 diabetes mellitus, lupus nephritis, and IgA nephropathy [17, 18, 20]. One study showed that inhibition of periostin expression was associated with decreased renal inflammation and fibrosis both in vitro and in vivo [19].…”

Section: Introductionmentioning

confidence: 99%

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Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

et al. 2017

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Background: Periostin is responsible for tissue regeneration, fibrosis, and wound healing via its interaction with integrin. Recently, the role of periostin has been shown to contribute to fibrosis in chronic kidney disease. We investigated the role of periostin and the effect of periostin blockade in renal fibrogenesis. Methods: We investigated the function of periostin in vivo in wild-type and periostin-null mice (Postn-KO) in a unilateral ureteral obstruction (UUO) model. For the in vitro experiments, primary cultured inner medullary collecting duct cells from the wild-type and Postn-KO mice were used. Results: Periostin expression was strongly induced by UUO in the wild-type mice. UUO induced renal fibrosis and morphological changes in the obstructed kidney of wild-type mice, whereas global knockout of periostin reduced fibrosis induced by UUO and improved kidney structure. Fibrosis- and inflammation-related mRNA were significantly induced in the wild-type mice and were decreased in the Postn-KO mice. Additionally, α-smooth muscle actin expression was increased following the administration of recombinant periostin in vitro. The effect of periostin blockade was examined using 2 methods. The integrin blockade peptide decreased fibrosis-related gene expression in in vitro experiments. Anti-periostin polyclonal antibody attenuated renal fibrosis induced by UUO through changes in transforming growth factor-β signaling and the inflammatory and apoptotic pathways. Conclusion: Periostin is a marker of renal fibrosis and may augment the progression of fibrogenesis as an extracellular matrix protein. Periostin blockade effectively attenuated renal fibrogenesis. Thus, periostin inhibition may be a therapeutic strategy for the amelioration of renal disease progression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

et al. 2017

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“…In parallel, periostin was found de novo expressed in biopsies from patients with various renal diseases, including diabetes, lupus nephritis, IgA nephropathy, and focal segmental glomerulosclerosis. The protein was over-expressed in areas with periglomerular or interstitial fibrosis and its expression levels were associated with the degree of histological damage and the decline of glomerular filtration rate (25, 28–31). Several studies also reported the detection of elevated periostin levels in the urine of CKD patients, which were correlated with the stage of the disease and could predict worsening renal outcomes (29–32).…”

Section: Periostin In Ckdmentioning

confidence: 99%

“…Moreover, periostin is secreted and can be easily detected in a non-invasive manner in plasma or urine samples. The normal levels of periostin in the plasma of healthy donors range between 10 and 60 ng/ml (57, 58), while in urine it is less than 1 ng/mg creatinine (29, 31, 32). Of note, although its expression in normal urine is negligible, it was shown to substantially increase and correlate with the severity of the disease in several types of CKD (27–30).…”

Section: Potential Of Periostin and Ddr1 As Biomarkers Or Therapeuticmentioning

confidence: 99%

Periostin and Discoidin Domain Receptor 1: New Biomarkers or Targets for Therapy of Renal Disease

Prakoura

Chatziantoniou

2017

Front. Med.

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Chronic kidney disease (CKD) can be a life-threatening condition, which eventually requires renal replacement therapy through dialysis or transplantation. A lot of effort and resources have been invested the last years in the identification of novel markers of progression and targets for therapy, in order to achieve a more efficient prognosis, diagnosis, and treatment of renal diseases. Using experimental models of renal disease, we identified and studied two promising candidates: periostin, a matricellular protein with high expression in bone and dental tissues, and discoidin domain receptor 1 (DDR1), a transmembrane collagen receptor of the tyrosine kinase family. Both proteins are inactive in physiological conditions, while they are highly upregulated during development of renal disease and are primarily expressed at the sites of injury. Further studies demonstrated that both periostin and DDR1 are involved in the regulation of inflammation and fibrosis, two major processes implicated in the development of renal disease. Targeting of either protein by genetic deletion or pharmacogenetic inhibition via antisense oligonucleotides highly attenuates renal damage and preserves renal structure and function in several animal models. The scope of this review is to summarize the existing evidence supporting the role of periostin and DDR1 as novel biomarkers and therapeutic targets in CKD.

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Periostin Induces Epithelial‐Mesenchymal Transition via p38‐MAPK Pathway in Human Renal Tubular Cells by High Glucose

Xiong,

Feng,

Ding

2024

Immunity Inflam & Disease

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BackgroundPeriostin mediates inflammation and fibrosis by regulating extracellular matrix adhesion, migration, and differentiation in multiple organ diseases. Studies have shown periostin mainly located in the dilated mesangium, tubulointerstitial and fibrotic regions of the diabetic kidney disease, which was negatively correlated with renal function. However, the underlying mechanism remains poorly explored.MethodsThe expression of periostin in HK‐2 cells was investigated under high glucose and high concentration of TGF‐β1. The signaling pathway of periostin involved in epithelial‐mesenchymal transdifferentiation of HK‐2 cells was also validated. The expression of periostin were investigated by RT‐PCR, western blot analysis and immunofluorescence assays with different concentrations of glucose and TGF‐β1. The expression of E‐Cad, α‐SMA and p38 proteins were also detected. The effects of periostin, E‐Cad, and α‐SMA in high glucose were investigated by p38 inhibitors. To demonstrate the interaction among periostin, p38 and EMT markers, periostin under high glucose and high TGF‐β1 was knocked down, resulting p38 and phosphorylated p38 was evaluated.ResultsThe combined of high glucose (HG, 22 mmol/L) and high TGF‐β1 (10 ng/mL) upregulated the expression of periostin obviously, stimulating the expression of α‐SMA and p38 while inhibiting the expression of E‐Cad. p38 inhibitors reduced the expression of periostin and α‐SMA while promoted E‐Cad protein expression in HK‐2 cells under HG conditions. Additionally, p38‐MAPK signal pathway was involved in epithelial‐mesenchymal transition of human renal tubules in high glucose environment. Significant, knockdown periostin expression effectively inhibited the expression of p38 and phosphorylated p38 under the combination of HG and high TGF‐β1, verifying the interaction of periostin with the p38‐MAPK signaling pathway.ConclusionPeriostin, a downstream factor of TGF‐β1, is positively regulated by TGF‐β1 under HG condition, affecting the epithelial‐interstitial differentiation of HK‐2 cells via p38‐MAPK signaling pathway. Therefore, periostin may serve as a biomarker of renal fibrosis in diabetic kidney disease.

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Urinary Periostin Excretion Predicts Renal Outcome in IgA Nephropathy

Cited by 32 publications

References 26 publications

Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

Periostin and Discoidin Domain Receptor 1: New Biomarkers or Targets for Therapy of Renal Disease

Periostin Induces Epithelial‐Mesenchymal Transition via p38‐MAPK Pathway in Human Renal Tubular Cells by High Glucose

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