<i>Periostin</i> is expressed within the developing teeth at the sites of epithelial–mesenchymal interaction

Kruzynska-Frejtag, Agnieszka; Wang, Jian; Maeda, Manabu; Rogers, Rhonda; Krug, Edward L.; Hoffman, Stanley; Markwald, Roger R.; Conway, Simon J.

doi:10.1002/dvdy.10453

Cited by 135 publications

(131 citation statements)

References 59 publications

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“…In doing so, it could provide a framework for attachment and spreading of the migrating cells that are undergoing the EMT early on in valvulogenesis. This hypothesis is consistent with the cells of the tooth mesenchyme that also highly express periostin and undergo an EMT (Kruzynska-Frejtag et al, 2004). During cardiovascular development initially, periostin is expressed in response to signaling from the BMP and TGF-␤ family of growth factors (Horiuchi et al, 1999;Ji et al, 2000;Hall et al, 2001;Kruzynska-Frejtag et al, 2001Lindner et al, 2004).…”

Section: Resultssupporting

confidence: 78%

Immunolocalization of chick periostin protein in the developing heart

et al. 2005

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The process that cardiac cushions undergo to form the mature septa and valves of the adult heart is poorly understood. Periostin is an extracellular molecule that is expressed during cushion mesenchyme formation and throughout valvulogenesis. Once thought to be an osteoblast-specific factor, studies have shown this molecule is antiosteogenic. We have produced an antibody to chicken periostin and examined periostin's localization in the developing avian heart. This antibody recognized proteins from chick heart lysates around 90 kD molecular weight as predicted from the chick periostin mRNA and other periostin orthologs. Periostin immunolocalization was first evident as fibrous strands in the cushion mesenchyme. At HH25, periostin was detected on the basal surface of the trabecular endothelium and also on the endocardial epithelium of the atrioventricular cushion. We hypothesize that periostin may function in the organization of extracellular matrix molecules, providing cues necessary for attachment and spreading during the epithelialto-mesenchymal transitions of the endocardial epithelium. Enhanced secretion of periostin in the region of delamination may directly or indirectly promote change in the myocardium that precedes or mediates delamination of the leaflet. At later stages of development (HH34-38), periostin was seen predominantly in the fibrous regions of the heart, such as the left atrioventricular valve (LAV), annulus, cardiac skeleton, and adventitia. We propose that periostin is induced by sheer stress and may be an essential molecular component for structures of the heart that undergo mechanical stress or tension during the cardiac cycle.

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Section: Resultssupporting

confidence: 78%

Immunolocalization of chick periostin protein in the developing heart

et al. 2005

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“…Rabbit antiperiostin antibody (1:500; ref. 69), rat anti-Ki67 antibody (1:100, Dako), rabbit anti-fibroblast-specific protein 1 antibody (1:100, Dako), and FITCconjugated mouse anti-α-smooth muscle actin antibody (1:1,000, SigmaAldrich) were used as primary antibodies. Sections were washed in PBS and then incubated with Alexa Fluor 488-or 594-conjugated secondary antibodies.…”

Section: Figurementioning

confidence: 99%

Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β

Teekakirikul¹,

Eminaga²,

Toka³

et al. 2010

J. Clin. Invest.

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Mutations in sarcomere protein genes can cause hypertrophic cardiomyopathy (HCM), a disorder characterized by myocyte enlargement, fibrosis, and impaired ventricular relaxation. Here, we demonstrate that sarcomere protein gene mutations activate proliferative and profibrotic signals in non-myocyte cells to produce pathologic remodeling in HCM. Gene expression analyses of non-myocyte cells isolated from HCM mouse hearts showed increased levels of RNAs encoding cell-cycle proteins, Tgf-β, periostin, and other profibrotic proteins. Markedly increased BrdU labeling, Ki67 antigen expression, and periostin immunohistochemistry in the fibrotic regions of HCM hearts confirmed the transcriptional profiling data. Genetic ablation of periostin in HCM mice reduced but did not extinguish non-myocyte proliferation and fibrosis. In contrast, administration of Tgf-β-neutralizing antibodies abrogated non-myocyte proliferation and fibrosis. Chronic administration of the angiotensin II type 1 receptor antagonist losartan to mutation-positive, hypertrophynegative (prehypertrophic) mice prevented the emergence of hypertrophy, non-myocyte proliferation, and fibrosis. Losartan treatment did not reverse pathologic remodeling of established HCM but did reduce nonmyocyte proliferation. These data define non-myocyte activation of Tgf-β signaling as a pivotal mechanism for increased fibrosis in HCM and a potentially important factor contributing to diastolic dysfunction and heart failure. Preemptive pharmacologic inhibition of Tgf-β signals warrants study in human patients with sarcomere gene mutations.

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“…Originally termed osteoblast specific factor-2 (OSF-2), it was renamed periostin due localized expression in the periosteum and the periodontal ligament (Kruzynska-Frejtag et al 2004). In humans, the periostin gene is located on chromosome 13, at map position 13q13.3, and the protein is 835 amino acids in size.…”

Section: Periostin: a Novel Matricellular Proteinmentioning

confidence: 99%

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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Periostin is expressed within the developing teeth at the sites of epithelial–mesenchymal interaction

Cited by 135 publications

References 59 publications

Immunolocalization of chick periostin protein in the developing heart

Immunolocalization of chick periostin protein in the developing heart

Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β

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

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