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Membrane channel gene expression in costal cartilage from patients with chest wall deformities
Author(s) -
Asmar Anthony,
BarrettJolley Richard,
Kelly Robert,
Tanaz Royena,
Stacey Michael
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1224.39
Subject(s) - rib cage , costal cartilage , cartilage , pectus excavatum , chondrocyte , medicine , anatomy , pectus carinatum , sternum , ion channel , microbiology and biotechnology , osteoarthritis , pathology , biology , receptor , alternative medicine
Chondrocytes form permanent cartilagein joints and ribs. Although much work has been undertaken on joint cartilage with respect to osteoarthritis, little is known about rib, or costal, cartilage. Inherited disorders of costal cartilage include pectus excavatum(PE) and pectus carinatum (PC), where the sternum is either depressed towards the spine, or protrudes outwardly forming a ‘pigeon chest’ respectively. In severe case there are profound consequences on heart and lung function. The occurrence of these disorders is approximately 1 in 400–1,000 with a strong male bias. Key to chondrocyte function is the ability to respond to mechanical loads with changes of metabolic activity. This mechano transduction property is, in part, mediated through the activity of a range of constitutively expressed transmembrane channels; ion channels, gap junction proteins, and porins. Appropriate expression of ion channels has been shown essential for production of extracellular matrix and differential expression of transmembrane channels is correlated to other musculoskeletal diseases such as osteoarthritis and Albers‐Schönberg. In this study the objective was to measure consistency of gene expression between channelomes of chondrocytes from patients with chest wall deformities compared to apparentlynormal samples of costal cartilage obtained from individuals with no known history of chest wall deformity. Gene expression was also compared to myocardial cells with well‐defined channelome expression. In our preliminary data we found 23 genes for different ion channels commonly expressed between costal chondrocytes. Interestingly, there were five ion channel genes observed which are characteristic to chondrocytes from chest wall deformities and five observed only in control chondrocytes. mRNA expression of the gap junction/innexin‐like genes;Panx1, Cx43 and Cx45 was also detected. In conclusion , this data highlights similarities and differences between chondrocyte membrane channel gene expressions in cells derived from patients versus control cost alcartilage. Overall, the data shows high expression of a range of mechanically and metabolically sensitive membrane channels suggesting that chondrocytemechanotransduction may play an important role in chest wall deformity. Support or Funding Information Research reported in this publication was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institute of Health under the award number R21AR063334. The content is solely the responsibility of the authors and does not necessarily represent the views of the NIH. We also acknowledge partial support from the Breeden Adams Foundation of Norfolk, VA, USA.