Angiotensin II increases periostin expression via Ras/p38 MAPK/CREB and ERK1/2/TGF-β1 pathways in cardiac fibroblasts

Li, Li; Fan, Daiming; Wang, Cheng; Wang, Jinyu; Cui, Xiaojie; Wu, Dan; Zhou, Yun; Wu, Li‐Ling

doi:10.1093/cvr/cvr067

Cited by 152 publications

(112 citation statements)

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“…Twist was shown to bind and induce periostin promoter activity in preosteoblasts, whereas YY1 was found to bind on a conserved enhancer region on periostin promoter, regulating tissue-specific periostin expression in the cardiac cushion mesenchyme. 18,19 Our bioinformatics analysis revealed the presence of several putative proinflammatory transcription factor binding sites on periostin promoter, whereas transcription factor binding sites of the classic TGF-b1 signaling pathway, which has been shown to upregulate periostin in vitro, 1,5,8 were rare. In luciferase assays and at the endogenous gene level, we showed that proinflammatory transcription factors such as NFkΒ (p65), c-Jun, and STAT1 directly induced periostin promoter activity or gene expression.…”

Section: Discussionmentioning

confidence: 91%

“…[3][4][5] Interaction of periostin with cell-surface integrins avb3 and avb5 has been associated with increased adhesion and migration of cancer cells and vascular smooth muscle cells (SMCs). 6,7 Periostin is highly induced in vitro by TGF-b1, 1,5,8 and it was also found to be upregulated by angiotensin II in cardiac fibroblasts. 8 IL-4 and IL-13 increased periostin in lung fibroblasts and bronchial epithelial cells, associating its induction with asthma.…”

mentioning

confidence: 99%

“…6,7 Periostin is highly induced in vitro by TGF-b1, 1,5,8 and it was also found to be upregulated by angiotensin II in cardiac fibroblasts. 8 IL-4 and IL-13 increased periostin in lung fibroblasts and bronchial epithelial cells, associating its induction with asthma. 9 Periostin has been found to be upregulated in renal disease models and kidney biopsy specimens.…”

mentioning

confidence: 99%

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NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

Prakoura

Kavvadas

Kormann

et al. 2016

JASN

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De novo expression in the kidney of periostin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal disease. In this study, we investigated the mechanism(s) of induction and the role of periostin in renal disease. Using a combination of bioinformatics, reporter assay, and chromatin immunoprecipitation analyses, we found that NFkB and other proinflammatory transcription factors induce periostin expression in vitro and that binding of these factors on the periostin promoter is enriched in glomeruli during experimental GN. Mice lacking expression of periostin displayed preserved renal function and structure during GN. Furthermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN reversed already established proteinuria, diminished tissue inflammation, and improved renal structure. Lack of periostin expression also blunted the de novo renal expression of integrin-b3 and phosphorylation of focal adhesion kinase and AKT, known mediators of integrin-b3 signaling that affect cell motility and survival, observed during GN in wild-type animals. In vitro, recombinant periostin increased the expression of integrin-b3 and the concomitant phosphorylation of focal adhesion kinase and AKT in podocytes. Notably, periostin and integrin-b3 were highly colocalized in biopsy specimens from patients with inflammatory GN. These results demonstrate that interplay between periostin and renal inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through downstream activation of integrin-b3 signaling. Targeting periostin may be a novel therapeutic strategy for treating CKD.

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

mentioning

confidence: 99%

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NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

Prakoura

Kavvadas

Kormann

et al. 2016

JASN

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“…MAPKs are pivotal mediators of the effects of Ang II on tissue structure by increasing TGF‐β1 expression, leading to atrial fibrosis 38, 39, 40. TGF‐β1 is a cytokine that regulates cell proliferation, apoptosis, migration, and synthesis of ECM, such as fibronectin and collagen in the atrium 41, 42.…”

Section: Discussionmentioning

confidence: 99%

Xanthine Oxidase Inhibitor Allopurinol Prevents Oxidative Stress‐Mediated Atrial Remodeling in Alloxan‐Induced Diabetes Mellitus Rabbits

Yang

Zhao

Qiu

et al. 2018

JAHA

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BackgroundThere are several mechanisms, including inflammation, oxidative stress and abnormal calcium homeostasis, involved in the pathogenesis of atrial fibrillation. In diabetes mellitus (DM), increased oxidative stress may be attributable to higher xanthine oxidase activity. In this study, we examined the relationship between oxidative stress and atrial electrical and structural remodeling, and calcium handling abnormalities, and the potential beneficial effects of the xanthine oxidase inhibitor allopurinol upon these pathological changes.Methods and ResultsNinety rabbits were randomly and equally divided into 3 groups: control, DM, and allopurinol‐treated DM group. Echocardiographic and hemodynamic assessments were performed in vivo. Serum and tissue markers of oxidative stress and atrial fibrosis, including the protein expression were examined. Atrial interstitial fibrosis was evaluated by Masson trichrome staining. ICaL was measured from isolated left atrial cardiomyocytes using voltage‐clamp techniques. Confocal microscopy was used to detect intracellular calcium transients. The Ca2+ handling protein expression was analyzed by Western blotting. Mitochondrial‐related proteins were analyzed as markers of mitochondrial function. Compared with the control group, rabbits with DM showed left ventricular hypertrophy, increased atrial interstitial fibrosis, oxidative stress and fibrosis markers, ICaL and intracellular calcium transient, and atrial fibrillation inducibility. These abnormalities were alleviated by allopurinol treatment.ConclusionsAllopurinol, via its antioxidant effects, reduces atrial mechanical, structural, ion channel remodeling and mitochondrial synthesis abnormalities induced by DM‐related increases in oxidative stress.

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“…Studies in a model of cardiac fibrosis indicated that periostin may act as a downstream mediator of Ang II signaling through complex interactions that involve p38/ CREB and erk/TGF-β pathways [14]. Additionally, lung fibroblasts from periostin-/-animals had an impaired response to TNF-α, and they failed to produce chemokines and pro-inflammatory cytokines, indicating that periostin could mediate both the inflammatory and the fibrotic process [15].…”

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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Angiotensin II increases periostin expression via Ras/p38 MAPK/CREB and ERK1/2/TGF-β1 pathways in cardiac fibroblasts

Abstract: The activation of the Ras/p38 MAPK/CREB pathway is required for AngII-induced periostin expression. ERK1/2 also participates in AngII-induced periostin expression by regulating TGF-β1/Smad signalling.

Cited by 152 publications

References 36 publications

NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

Xanthine Oxidase Inhibitor Allopurinol Prevents Oxidative Stress‐Mediated Atrial Remodeling in Alloxan‐Induced Diabetes Mellitus Rabbits

New Targets for End-Stage Chronic Kidney Disease Therapy

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