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    • "Periostin, originally named osteoblast-specific factor 2 (OSF-2), was first identified in a mouse osteoblastic cell line as a cell adhesion protein (Takeshita et al., 1993; Horiuchi et al., 1999) and was recently classified as a novel matricellular protein (Norris et al., 2007; Hamilton, 2008; Ruan et al., 2009). The generation of periostin-knockout mice provided further insight into its functions in embryonic development (Rios et al., 2005; Kii et al., 2006; Norris et al., 2008). Current studies in animal models and patients demonstrate that periostin is involved in the pathobiology of various diseases, including fibrosis, arthritis, atherosclerosis and other inflammatory diseases, as well as tumorigenesis and metastasis (Ruan et al., 2009; Kudo, 2011; Conway et al., 2014). "
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    ABSTRACT: The behavior and fate of cells in tissues largely rely upon their cross-talk with the tissue microenvironment including neighboring cells, the extracellular matrix (ECM), and soluble cues from the local and systemic environments. Dysregulation of tissue microenvironment can drive various inflammatory diseases and tumors. The ECM is a crucial component of tissue microenvironment. ECM proteins can not only modulate tissue microenvironment but also regulate the behavior of surrounding cells and the homeostasis of tissues. As a nonstructural ECM protein, periostin is generally present at low levels in most adult tissues; however, periostin is often highly expressed at sites of injury or inflammation and in tumors within adult organisms. Current evidence demonstrates that periostin actively contributes to tissue injury, inflammation, fibrosis and tumor progression. Here, we summarize the roles of periostin in inflammatory and tumor microenvironments.
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    ABSTRACT: Most nonsyndromic congenital heart malformations (CHMs) in humans are multifactorial in origin, although an increasing number of monogenic cases have been reported recently. We describe here four new families with presumed autosomal dominant inheritance of left ventricular outflow tract obstruction (LVOTO), consisting of hypoplastic left heart (HLHS) or left ventricle (HLV), aortic valve stenosis (AS) and bicuspid aortic valve (BAV), hypoplastic aortic arch (HAA), and coarctation of the aorta (CoA). LVOTO in these families shows a wide clinical spectrum with some family members having severe anomalies such as hypoplastic left heart, and others only minor anomalies such as mild aortic valve stenosis. This supports the suggestion that all anomalies of the LVOTO spectrum are developmentally related and can be caused by a single gene defect.
    American Journal of Medical Genetics Part A 04/2005; 134A(2):171-9. DOI:10.1002/ajmg.a.30601 · 2.16 Impact Factor
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    ABSTRACT: Considerable progress has been made in recent years toward elucidating a conceptual framework that integrates the dynamic functional structure, mechanical properties, and pathobiological behavior of the cardiac valves. This communication reviews the evolving paradigm of a continuum of heart valve structure, function, and pathobiology and explores its implications. Specifically, we discuss (1) the interactions of valve biology and biomechanics (eg, correlations of function with structure at the cell, tissue, and organ levels and mechanical considerations, development, endothelial cell and interstitial cell biology, extracellular matrix biology, homeostasis, and adaptation to environmental change); (2) mechanisms of disease (eg, valve cell and matrix pathobiology in congenital anomalies, aortic valve calcification, and mitral valve prolapse); (3) considerations in replacement and repair (eg, cell/matrix biology of tissue valve substitutes and their degeneration and durability of repairs); and (4) the potential for tissue engineering approaches to therapeutic regeneration of the cardiac valves. Opportunities for research and clinical translation are highlighted.
    Circulation 11/2008; 118(18):1864-80. DOI:10.1161/CIRCULATIONAHA.108.805911 · 14.43 Impact Factor
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