A Novel Role of the Sympatho-Adrenergic System in Regulating Valve Calcification

Osman, Lana; Chester, Adrian H.; Sarathchandra, Padmini; Latif, Najma; Meng, Wenfang; Taylor, Patricia M.; Yacoub, Magdi H.

doi:10.1161/circulationaha.106.681072

Cited by 32 publications

(32 citation statements)

References 24 publications

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“…Because elevated periostin expression is present following adult myocardial hypertrophy, 10 infarction, 27 arterial injury, 15 and valve calcification, 28 we examined its expression in both normal and heart failure models to assess when and where periostin elevation occurs. To efficiently distinguish cardiomyocytes from the noncardiomyocyte cells, we made use of the ␣MHC-EGFP reporter mice 19 expressing EGFP exclusively in cardiac muscle.…”

Section: Periostin Is Absent From Cardiomyocytes But Is Expressed Thrmentioning

confidence: 99%

Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart

Snider

Hinton

Rodríguez

et al. 2008

Circulation Research

286

314

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Abstract-The secreted periostin protein, which marks mesenchymal cells in endocardial cushions following epithelialmesenchymal transformation and in mature valves following remodeling, is a putative valvulogenesis target molecule. Indeed, periostin is expressed throughout cardiovascular morphogenesis and in all 4 adult mice valves (annulus and leaflets). Additionally, periostin is expressed throughout the fibrous cardiac skeleton and endocardial cushions in the developing heart but is absent from both normal and/or pathological mouse cardiomyocytes. Periostin (peri lacZ ) knockout mice exhibit viable valve disease, with neonatal lethality in a minority and latent disease with leaflet abnormalities in the viable majority. Surviving peri lacZ -null leaflets are truncated, contain ectopic cardiomyocytes and smooth muscle, misexpress the cartilage proteoglycan aggrecan, demonstrate disorganized matrix stratification, and exhibit reduced transforming growth factor-␤ signaling. Neonatal peri lacZ nulls that die (14%) display additional defects, including leaflet discontinuities, delamination defects, and deposition of acellular extracellular matrix. Assessment of collagen production, 3D lattice formation ability, and transforming growth factor-␤ responsiveness indicate periostin-deficient fibroblasts are unable to support normal valvular remodeling and establishment of a mature cardiac skeleton.

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Section: Periostin Is Absent From Cardiomyocytes But Is Expressed Thrmentioning

confidence: 99%

Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart

Snider

Hinton

Rodríguez

et al. 2008

Circulation Research

286

314

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“…The previous studies conducted on VHD have largely been observational, immunohistologic, and in vitro studies (8)(9)(10)(11)(12)(13). Although the onset of aortic valve stenosis has been reported in Smad6-deficient mice (14), in fibulin 4-deficient mice (15), and in humans with the NOTCH1 mutation (16), the abnormality has primarily been observed during cardiac valve development.…”

Section: Introductionmentioning

confidence: 99%

Periostin advances atherosclerotic and rheumatic cardiac valve degeneration by inducing angiogenesis and MMP production in humans and rodents

Hakuno

Kimura²,

Yoshioka³

et al. 2010

J. Clin. Invest.

174

135

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Valvular heart disease (VHD) is the term given to any disease process involving one or more of the heart valves. The condition can be congenital or acquired, for example as a result of atherosclerosis or rheumatic fever. Despite its clinical importance, the molecular mechanisms underlying VHD remain unknown. We investigated the pathophysiologic role and molecular mechanism of periostin, a protein that plays critical roles in cardiac valve development, in degenerative VHD. Unexpectedly, we found that periostin levels were drastically increased in infiltrated inflammatory cells and myofibroblasts in areas of angiogenesis in human atherosclerotic and rheumatic VHD, whereas periostin was localized to the subendothelial layer in normal valves. The expression patterns of periostin and chondromodulin I, an angioinhibitory factor that maintains cardiac valvular function, were mutually exclusive. In WT mice, a high-fat diet markedly increased aortic valve thickening, annular fibrosis, and MMP-2 and MMP-13 expression levels, concomitant with increased periostin expression; these changes were attenuated in periostin-knockout mice. In vitro and ex vivo studies revealed that periostin promoted tube formation and mobilization of ECs. Furthermore, periostin prominently increased MMP secretion from cultured valvular interstitial cells, ECs, and macrophages in a cell type-specific manner. These findings indicate that, in contrast to chondromodulin I, periostin plays an essential role in the progression of cardiac valve complex degeneration by inducing angiogenesis and MMP production.

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“…NE can cause a potent contraction of smooth muscle cells through the stimulation of specific receptor subtypes in equine aortic valve 9,10 . There are more known adrenoceptor subtypes, a number of which have been found in human heart valve tissue: α1, α2, β1 and β2 adrenoceptors 10,11 . Williams TH et al 3 reported that rat mitral valves had been shown to display spontaneous contraction-like movements localized to the leaflet itself, immediately after being dissected from the heart, which was enhanced by addition of norepinephrine (NE) in a dose-dependent fashion.…”

Section: Discussionmentioning

confidence: 99%

Regulação autonômica das propriedades mecânicas em bioprótese valvar porcina

Zhao

2012

Arq. Bras. Cardiol.

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A Novel Role of the Sympatho-Adrenergic System in Regulating Valve Calcification

Cited by 32 publications

References 24 publications

Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart

Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart

Periostin advances atherosclerotic and rheumatic cardiac valve degeneration by inducing angiogenesis and MMP production in humans and rodents

Regulação autonômica das propriedades mecânicas em bioprótese valvar porcina

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