Periostin and periostin-like factor in the human heart: possible therapeutic targets

Litvin, Judith; Blagg, Andrew G; Mu, Anbin; Matiwala, Sunil; Montgomery, Michael T.; Berretta, Remus; Houser, Steven R.; Margulies, Kenneth B.

doi:10.1016/j.carpath.2005.09.001

Cited by 61 publications

(60 citation statements)

References 36 publications

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“…Periostin is a secreted protein involved in bone formation and cell-cell adhesion. It is upregulated in the Syrian hamster model of heart failure (69) and expressed in cardiac fibroblasts and implicated in cardiac dysfunction (38). The overexpression of periostin causes LV dilation and an increase in collagen deposition (30).…”

Section: Continuedmentioning

confidence: 99%

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Urashima

Zhao²,

Wagner³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

116

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physiological characterization of RV remodeling in a murine model of pulmonary stenosis. Am J Physiol Heart Circ Physiol 295: H1351-H1368, 2008. First published June 27, 2008 doi:10.1152/ajpheart.91526.2007 dysfunction is a common long-term complication in patients after the repair of congenital heart disease. Previous investigators have examined the cellular and molecular mechanisms of left ventricular (LV) remodeling, but little is known about the stressed RV. Our purpose was to provide a detailed physiological characterization of a model of RV hypertrophy and failure, including RV-LV interaction, and to compare gene alterations between afterloaded RV versus LV. Pulmonary artery constriction was performed in 86 mice. Mice with mild and moderate pulmonary stenosis (PS) developed stable hypertrophy without decompensation. Mice with severe PS developed edema, decreased RV function, and high mortality. Tissue Doppler imaging demonstrated septal dyssynchrony and deleterious RV-LV interaction in the severe PS group. Microarray analysis showed 196 genes with increased expression and 1,114 with decreased expression. Several transcripts were differentially increased in the afterloaded RV but not in the afterloaded LV, including clusterin, neuroblastoma suppression of tumorigenicity 1, Dkk3, Sfrp2, formin binding protein, annexin A7, and lysyl oxidase. We have characterized a murine model of RV hypertrophy and failure, providing a platform for studying the physiological and molecular events of RV remodeling. Although the molecular responses of the RV and LV to afterload stress are mostly concordant, there are several key differences, which may represent targets for RV failure-specific therapy. gene expression; right ventricle; tetralogy of Fallot THE RIGHT VENTRICLE IS UNIQUELY at risk in patients with complex congenital heart disease involving right-sided obstructive lesions (e.g., tetralogy of Fallot, tetralogy/pulmonary atresia) and in patients with systemic right ventricles (1,40,46). Increased stress on the right ventricle in the form of increased hemodynamic loading (pressure and/or volume) may result in abnormalities in cardiac structure, function, metabolism, coronary perfusion, neurohormonal activation, and molecular signaling. These stresses lead to both adaptive and maladaptive structural and molecular remodeling of the right ventricle and deleterious effects on the left ventricle through ventricular-ventricular interaction and may limit long-term survival (3,7,29,42). For many of these patients, detrimental conditions for the right ventricle exist throughout life, even after successful repair or palliation. As surgical techniques for the primary repair of complex forms of congenital heart disease improve, long-term survival and quality of life will depend on our ability to preserve long-term right ventricular (RV) function. Decisions regarding the ideal time for surgical reintervention will need to be based on more quantitative rather than qualitative measures.Developing a better understanding of the molecu...

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Section: Continuedmentioning

confidence: 99%

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Urashima

Zhao²,

Wagner³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

116

View full text Add to dashboard Cite

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“…1). Although recent reports suggested that in mice, spliced variants of periostin play crucial roles in adult cardiac myocyte growth following mechanical overload (21) and in osteoblast differentiation (22), the relationship between alternative splicing of periostin and human carcinogenesis has not yet been elucidated. In the present study, to clarify the role of alternative splicing of periostin in human bladder carcinogenesis, we investigated whether alternative splicing events actually occur in bladder cancer tissues and identified the role of spliced variants of periostin in the invasiveness and metastasis of cancer cells.…”

Section: Role Of Alternative Splicing Of Periostin In Human Bladder Cmentioning

confidence: 99%

Role of alternative splicing of periostin in human bladder carcinogenesis

Kim

Isono²,

Tambe³

et al. 2008

Int J Oncol

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Abstract.We have previously reported that the expression of periostin mRNA is significantly repressed in human bladder cancer tissues, and that periostin plays a role as a suppressive factor for invasion and metastasis in the progression of human bladder cancers. In this study, to clarify the role of alternative splicing of periostin in human bladder carcinogenesis, we examined the expression of wild-type (WT) and spliced variants of periostin mRNA in normal bladder and bladder cancer tissues. Although both WT and spliced periostin mRNA were expressed in all normal bladder tissues examined, no WT periostin mRNA was detected in the examined transitional cell carcinomas (TCCs) of the bladder (0/23) or in bladder cancer cell lines (0/6). Spliced variants of periostin were detected in 48% (11/23) of TCC tissues and 33% (2/6) of bladder cancer cell lines. Two types of spliced periostin (Variants I and II) were successfully isolated from bladder cancer tissues, but Variant I, which is predominantly expressed in bladder cancer tissues, did not show suppressor activity on in vitro invasiveness and in vivo metastasis of cancer cells. Immunohistochemical analysis indicated that strong belt-like expression of periostin protein was observed in the stroma just beneath the normal bladder epithelium, while it was mostly attenuated in bladder cancer tissues. These results indicate that the loss of WT periostin by down-regulation and/or alternative splicing, which produces Variant I, is closely correlated with the development of bladder cancer.

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“…Equal protein from each sample (100 g/lane) was separated by PAGE and the proteins transferred to nitrocellulose. The blots were probed with anti-PLF-specific antibody (18), stripped, and reprobed with anti-GAPDH as a loading control. Western blots were performed on proteins obtained from cells treated as described above in three separate experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Considering the role of PLF and periostin in remodeling (15,(17)(18)(19), we hypothesized that PLF would play a role in VSMC activation and in the development of vascular restenosis. Therefore, we challenged cultured, primary human VSMCs with cytokines and growth factors to determine whether PLF was responsive to these compounds.…”

Section: Plf Mrna and Protein Are Expressed In Activated Vsmcsmentioning

confidence: 99%

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Expression and function of periostin-like factor in vascular smooth muscle cells

Litvin¹,

Chen²,

Keleman³

et al. 2007

American Journal of Physiology-Cell Physiology

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In injured blood vessels activated vascular smooth muscle cells (VSMCs) migrate from the media to the intima, proliferate and synthesize matrix proteins. This results in occlusion of the lumen and detrimental clinical manifestations. We have identified a novel isoform of the periostin family of proteins referred to as periostin-like factor (PLF). PLF expression in VSMCs was increased following treatment with mitogenic compounds, suggesting that PLF plays a role in VSMC activation. Correspondingly, proliferation of the cells was significantly reduced with anti-PLF antibody treatment. PLF expression increased VSMC migration, an essential cellular process leading to vascular restenosis after injury. PLF protein was localized to neointimal VSMC of rat and swine balloon angioplasty injured arteries, as well as in human arteries with transplant restenosis, supporting the hypothesis that PLF is involved in VSMC activation and vascular proliferative diseases. Taken together, these data suggest a role for PLF in the regulation of vascular proliferative disease.

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Periostin and periostin-like factor in the human heart: possible therapeutic targets

Cited by 61 publications

References 36 publications

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Role of alternative splicing of periostin in human bladder carcinogenesis

Expression and function of periostin-like factor in vascular smooth muscle cells

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