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Cited by 323

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

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

Open access
Snider, Paige, Hinton, Robert B., Moreno-Rodriguez, Ricardo A., Wang, Jian, Rogers, Rhonda, Lindsley, Andrew, Li, Fang, Ingram, David A., Menick, Donald, Field, Loren, Firulli, Anthony B., Molkentin, Jeffery D., Markwald, Roger, Conway, Simon J.·2008·Circulation Research

Abstract

The secreted periostin protein, which marks mesenchymal cells in endocardial cushions following epithelial–mesenchymal 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-β 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-β responsiveness indicate periostin-deficient fibroblasts are unable to support normal valvular remodeling and establishment of a mature cardiac skeleton. Furthermore, pediatric stenotic bicuspid aortic valves that have lost normal extracellular matrix trilaminar stratification have greatly reduced periostin. This suggests that loss of periostin results in inappropriate differentiation of mesenchymal cushion cells and valvular abnormalities via a transforming growth factor-β–dependent pathway during establishment of the mature heart. Thus, peri lacZ knockouts provide a new model of viable latent valve disease.

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Metadata

Authors
Snider, P., Hinton, R. B., Moreno-Rodriguez, R. A., Wang, J., Rogers, R., Lindsley, A., Li, F., Ingram, D. A., Menick, D., Field, L., Firulli, A. B., Molkentin, J. D., Markwald, R., & Conway, S. J.
Venue
Circulation Research
Published
2008-04-11
Volume
102
Issue
7
Pages
752-760
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2167149037
Cited by
323
References
41
FWCI
8.93
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart. https://app.cochat.ai/papers/10.1161/circresaha.107.159517
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Snider, P., Hinton, R. B., Moreno-Rodriguez, R. A., Wang, J., Rogers, R., Lindsley, A., Li, F., Ingram, D. A., Menick, D., Field, L., Firulli, A. B., Molkentin, J. D., Markwald, R., & Conway, S. J. (2008). Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart. Circulation Research. https://doi.org/10.1161/circresaha.107.159517

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