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(Circulation Research. 2008;103:914.)
© 2008 American Heart Association, Inc.

Editorials

Thar’s Tendons in Them Thar Valves!

D. Woodrow Benson

From the Division of Cardiology, Cincinnati Children’s Hospital, Ohio.

Correspondence to D. Woodrow Benson, Division of Cardiology, MLC 7042, Cincinnati Children’s Hospital, 3333 Burnet Ave, Cincinnati, OH 45229-3039. E-mail woody.benson@cchmc.org

See related article, pages 948–956

Key Words: cardiac development • cardiac valves • valve disease

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In this issue of Circulation Research, Levay et al report an in vivo requirement for scleraxis (scx) during murine valvulogenesis and demonstrate its role in cell lineage differentiation and matrix distribution in remodeling valve structures.¹ The scleraxis (Scx) gene encodes a basic helix–loop–helix transcription factor that is expressed in the progenitors and cells of all tendon tissues.² Recent studies have identified the specific regulatory pathway in which fibroblast growth factor activates the mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) signaling cascade to promote expression of scx, which, in turn, induces expression of tenascin as being shared by developing valves and limb buds.³ In initial studies in chick, Lincoln et al found a restricted pattern of scx expression, suggesting that atrioventricular (AV) valve precursor cells diversify into leaflets (cartilage-like) or chordae tendineae (tendon-like) to produce both a leaflet and supporting apparatus,⁴ as opposed to semilunar valve precursor cells that exhibit both cartilage- and tendon-like characteristics and diversify into cusps with an internal supporting apparatus.⁵ However, in the present study, Lincoln and colleagues identified high levels of scx expression in remodeling AV and semilunar valve structures from embryonic day (E)15.5 through postnatal stages; the biological significance of this apparent difference between chick and mouse is not known.

Levay et al¹ determined the in vivo function of scx using null mice (scx^–/–). Scx expression is not detected during early stages of valve development, and extracellular matrix (ECM) deposition appears normal in scx^–/– mice up to E16.5, suggesting . . . [Full Text of this Article]

Related Article:

Scleraxis Is Required for Cell Lineage Differentiation and Extracellular Matrix Remodeling During Murine Heart Valve Formation In Vivo

Agata K. Levay, Jacqueline D. Peacock, Yinhui Lu, Manuel Koch, Robert B. Hinton, Jr, Karl E. Kadler, and Joy Lincoln
Circ. Res. 2008 103: 948-956. [Abstract] [Full Text] [PDF]