Development of myotendinous‐like junctions that anchor cardiac valves requires fibromodulin and lumican |
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| Authors: | Loren E. Dupuis Lorna Doucette A. Kittrell Rice Ashton E. Lancaster Matthew G. Berger Shukti Chakravarti Christine B. Kern |
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| Affiliation: | 1. Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, South Carolina;2. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland |
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| Abstract: | Results : FMOD deficient mice and double deficient FMOD; LUM mice exhibited anomalies in regions where cardiac valve tissue interdigitates with adjacent muscle for support. Ectopic connective and/or myocardial tissue(s) was associated with the more severe cardiac valve anomalies in FMOD; LUM deficient mice. At postnatal day 0 (P0) there was an increase in the mesenchymal cell number in the regions where valve cusps anchor in FMOD; LUM deficient mice compared to WT. The cardiac valve anomalies correlated with the highest levels of FMOD expression in the heart and also where myotendinous junctions (MTJ) components biglycan, collagen type I alpha 1, and collagen type VI, are also localized. | |
| Keywords: | valve extracellular matrix fibromodulin lumican development myotendinous junction cardiac SLRP collagen |
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