Periostin: novel tissue and urinary biomarker of progressive renal injury induces a coordinated mesenchymal phenotype in tubular cells

Satirapoj, Bancha; Wang, Ying; Chamberlin, M; Dai, Tiane; LaPage, Janine; Phillips, Lynetta; Nast, Cynthia C.; Adler, Sharon G.

doi:10.1093/ndt/gfr670

Cited by 59 publications

(87 citation statements)

References 32 publications

(36 reference statements)

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“…Periostin is known to be expressed during renal development, but it is not expressed in the normal adult kidney [34]. Periostin is currently emerging as a marker of and therapeutic target for renal fibrosis, and related studies in various renal diseases have been published recently [13-19]. …”

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%

“…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]. 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].…”

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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“…13 Other investigators observed increased concentrations of urinary periostin in a small cohort of CKD patients. 14 We reported that periostin is highly upregulated during disease progression and inversely downregulated during regression in a model of hypertensive renal disease. 15 Although the above results indicate that periostin can be a new biomarker of renal disease progression, whether periostin participates in the development of CKD has not been examined.…”

mentioning

confidence: 90%

Inhibition of Periostin Expression Protects against the Development of Renal Inflammation and Fibrosis

Mael-Ainin

Abed

Conway

et al. 2014

Journal of the American Society of Nephrology

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Increased renal expression of periostin, a protein normally involved in embryonic and dental development, correlates with the decline of renal function in experimental models and patient biopsies. Because periostin has been reported to induce cell differentiation, we investigated whether it is also involved in the development of renal disease and whether blocking its abnormal expression improves renal function and/ or structure. After unilateral ureteral obstruction in wild-type mice, we observed a progressive increase in the expression and synthesis of periostin in the obstructed kidney that associated with the progression of renal lesions. In contrast, mice lacking the periostin gene showed less injury-induced interstitial fibrosis and inflammation and were protected against structural alterations. This protection was associated with a preservation of the renal epithelial phenotype. In vitro, administration of TGF-b to renal epithelial cells increased the expression of periostin several-fold, leading to subsequent loss of the epithelial phenotype. Furthermore, treatment of these cells with periostin increased the expression of collagen I and stimulated the phosphorylation of FAK, p38, and ERK 42/44. In vivo delivery of antisense oligonucleotides to inhibit periostin expression protected animals from L-NAME-induced renal injury. These data strongly suggest that periostin mediates renal disease in response to TGF-b and that blocking periostin may be a promising therapeutic strategy against the development of CKD.

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“…In addition, delivery of antisense oligonucleotides against periostin protected rats from the progression of renal disease in the L-NAME model [12]. Other investigators showed that periostinis overexpressed in additional experimental models of renal pathology and most importantly, it can be detected in the urine of human patients of CKD, even when albuminuria is within normal values [13].…”

Section: Periostinmentioning

confidence: 99%

New Targets for End-Stage Chronic Kidney Disease Therapy

Prakoura

Kavvadas

Chatziantoniou

2015

The Journal of Critical Care Medicine

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Severe forms of chronic kidney disease can lead to a critical, end-stage condition, requiring renal replacement therapy, which may involve a form of dialysis or renal transplantation. Identification and characterization of novel markers and/or targets of therapy that could be applied in these critically ill patients remains the focus of the current research in the field of critical care medicine and has been the objective of our studies for some years past. To this end, we used models of renal vascular disease, Ang II, L-NAME or mice overexpressing renin, treated with AT1 antagonists at different stages of progression, to create cohorts of animals during progression, reversal or escape from therapy. Transcriptomic analysis and comparisons were performed and genes were selected according to the following criteria: a) not previously described in the kidney, b) highly upregulated during progression and returning to the normal levels during reversal, and c) producing proteins that are either circulating or membrane receptors. The involvement of the selected genes in the mechanisms of renal disease was confirmed in additional models of renal disease, initiated in other compartments of the kidney such as glomeruli (administration of nephrotoxic serum) or the tubular interstitium (unilateral ureteral obstruction). The potential of the therapy was tested using mice lacking the expression of these genes and by in vivo administration of antisense oligonucleotides which blocked the transcription of the targeted genes. This strategy allowed the identification of periostin, an extracellular matrix protein normally involved in bone and tooth development, in addition to the discoidin domain receptor1 (DDR1) as potential targets of therapy against renal inflammation and fibrosis.

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Periostin: novel tissue and urinary biomarker of progressive renal injury induces a coordinated mesenchymal phenotype in tubular cells

Abstract: These data demonstrate that periostin is a mediator and marker of tubular dedifferentiation and a promising tissue and urine biomarker for kidney injury in experimental models and in clinical renal disease.

Cited by 59 publications

References 32 publications

Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

Experimental Inhibition of Periostin Attenuates Kidney Fibrosis

Inhibition of Periostin Expression Protects against the Development of Renal Inflammation and Fibrosis

New Targets for End-Stage Chronic Kidney Disease Therapy

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