Periostin is essential for cardiac healing after acute myocardial infarction

Shimazaki, Masashi; Nakamura, Kazuto; Kii, Isao; Kashima, Takeshi; Amizuka, Norio; Li, Minqi; Saito, Mitsuru; Fukuda, Keiichi; Nishiyama, Takashi; Kitajima, Satoshi; Saga, Yumiko; Fukayama, Masashi; Sata, Masataka; Kudo, Akira

doi:10.1083/jcb1802oia7

Cited by 123 publications

(223 citation statements)

References 17 publications

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“…28 In a model of acute myocardial infarction, periostin null mice exhibited impaired cardiac healing as a result of reduced myocardial stiffness and collagen fibril formation, whereas inducible overexpression of periostin protected mice from cardiac rupture. 29,30 The ability of periostin to interact and stabilize fibrillar collagens and other extracellular matrix molecules is probably a key event by which periostin controls extracellular matrix deposition and development of fibrosis. [3][4][5] We found de novo expressed periostin to colocalize and interact with integrin-b3 in glomeruli and vascular SMCs of NTS mice.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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

Prakoura

Kavvadas

Kormann

et al. 2016

JASN

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“…Thus far, periostin has been found in bone (Horiuchi et al 1999;Litvin et al 2004;Nakazawa et al 2004;Oshima et al 2002), skin Roy et al 2007;Tilman et al 2007), periodontal ligament (Horiuchi et al 1999;Kii and Kudo 2007;Kruzynska-Frejtag et al 2004;Lallier and Spencer 2007;Suzuki et al 2004), muscle injury (Goetsch et al 2003;Kudo et al 2004), vascular injury (Lindner et al 2005), myocardial infarction (Dorn 2007;Iekushi et al 2007;Oka et al 2007;Shimazaki et al 2008), epithelial ovarian cancer (Gillan et al 2002), colorectal cancer (Tai et al 2005), and pulmonary vascular remodeling (Li et al 2004;Woodruff et al 2007). Furthermore, periostin expression is known to be prominent in fibrotic conditions, including sub-epithelial fibrosis in bronchial asthma (Takayama et al 2006), as well as in bone marrow fibrosis (Oku et al 2008).…”

Section: Periostin: a Novel Matricellular Proteinmentioning

confidence: 99%

“…However, to date, the expression profile of periostin in the wound repair process has yet to be elucidated. Thus far, expression of periostin in tissue repair has been investigated predominantly within the vascular and cardiac systems (Dorn 2007;Kuhn et al 2007;Lindner et al 2005;Litvin et al 2007;Norris et al 2008a;Shimazaki et al 2008), and to a lesser extent in chronic dermal wounds (Roy et al 2007), muscle (Goetsch et al 2003), and bone fracture (Nakazawa et al 2004). Interestingly, the regulatory processes, including matricellular protein expression, responsible for normal development of bone, cartilage and cardiac tissue also play a major role in their pathogenesis in adults.…”

Section: Wound Repairmentioning

confidence: 99%

“…Periostin has been observed to increase the number of cardiomyocytes actively replicating DNA in rats after myocardial infarction (Kuhn et al 2007). In particular, periostin is expressed by cardiac fibroblasts where it interacts with integrins on cells likely modulating their behaviour during the remodeling process following infarct (Shimazaki et al 2008). However, it is still not clear if periostin acts on cardiomyocytes directly, or support cells only such as the cardiac fibroblasts (Dorn 2007).…”

Section: Wound Repairmentioning

confidence: 99%

“…Matricellular proteins are important during development, but are typically restricted to tissue remodeling and wound repair in the normal adult. Matricellular proteins interact with cell surface receptors such as integrins and are able to bind growth factors as well as to the structural components of the matrix such as collagen (Baril et al 2007;Butcher et al 2007;Gillan et al 2002;Shimazaki et al 2008). Based on this definition, several proteins have now been identified as matricellular proteins (Bornstein 2000), including connective tissue growth factors (Leask and Abraham 2006), thrombospondins Chen et al 2000), and galectins (Elola et al 2007;He and Baum 2006).…”

Section: Introductionmentioning

confidence: 99%

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Functional role of periostin in development and wound repair: implications for connective tissue disease

Hamilton

2008

Journal of Cell Communication and Signaling

175

191

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Integrity of the extracellular matrix (ECM) is essential for maintaining the normal structure and function of connective tissues. ECM is secreted locally by cells and organized into a complex meshwork providing physical support to cells, tissues, and organs. Initially thought to act only as a scaffold, the ECM is now known to provide a myriad of signals to cells regulating all aspects of their phenotype from morphology to differentiation. Matricellular proteins are a class of ECM related molecules defined through their ability to modulate cell–matrix interactions. Matricellular proteins are expressed at high levels during development, but typically only appear in postnatal tissue in wound repair or disease, where their levels increase substantially. Members of the CCN family, tenascin‐C, osteopontin, secreted protein acidic rich in cysteine (SPARC), bone sialoprotein, thrombospondins, and galectins have all been classed as matricellular proteins. Periostin, a 90 kDa secreted homophilic cell adhesion protein, was recently added to matricellular class of proteins based on its expression pattern and function during development as well as in wound repair. Periostin is expressed in connective tissues including the periodontal ligament, tendons, skin and bone, and is also prominent in neoplastic tissues, cardiovascular disease, as well as in connective tissue wound repair. This review will focus on the functional role of periostin in tissue physiology. Fundamentally, it appears that periostin influences cell behaviour as well as collagen fibrillogenesis, and therefore exerts control over the structural and functional properties of connective tissues in both health and disease. Periostin is a novel matricellular protein with close homology to Drosophila fasciclin 1. In this review, the functional role of periostin is discussed in the context of connective tissue physiology, in development, disease, and wound repair.

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GRK5‐mediated inflammation and fibrosis exert cardioprotective effects during the acute phase of myocardial infarction

et al. 2023

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During myocardial infarction (MI), cardiac cells at the infarcted area undergo cell death. In response, cardiac myofibroblasts, which are mainly differentiated from resident fibroblasts upon inflammation, produce extracellular matrix proteins such as collagen to fill the damaged areas of the heart to prevent cardiac rupture. In this study, we identified a cardioprotective role of G‐protein‐coupled receptor kinase 5 (GRK5) in MI. GRK5 expression was found to increase in the mouse heart after MI and was highly expressed in cardiac fibroblasts/myofibroblasts. In fibroblasts/myofibroblasts, GRK5 promoted the expression of inflammation‐related genes through nuclear factor‐κB activation, leading to an increase in the expression levels of fibrosis‐related genes. Bone marrow transfer experiments confirmed that GRK5 in fibroblasts/myofibroblasts, but not in infiltrated macrophages in the infarcted area, is mainly responsible for GRK5‐mediated inflammation in infarcted hearts. In addition, inflammation and fibrosis at the infarcted area were significantly suppressed in GRK5 knockout mice, resulting in increased mortality compared with that in wild‐type mice. These data indicate that GRK5 in cardiac fibroblasts/myofibroblasts promotes inflammation and fibrosis to ameliorate the damage after MI.

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Periostin is essential for cardiac healing after acute myocardial infarction

Cited by 123 publications

References 17 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

Functional role of periostin in development and wound repair: implications for connective tissue disease

GRK5‐mediated inflammation and fibrosis exert cardioprotective effects during the acute phase of myocardial infarction

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