Transforming growth factor beta3 increases chondrocyte proliferation and decreases apoptosis in murine cricoid cartilage in vitro.

OBJECTIVE: To determine if the luminal epithelium and/or exogenous transforming growth factor beta (TGFbeta) affects growth of the cricoid. DESIGN: Subglottises from 20 neonatal mice were subdivided into four groups: A, five subglottises with luminal epithelium grown in basic medium; B, five epithelium-free subglottises in basic medium; C, five epithelium-free subglottises in basic medium with supplemental TGFbeta1, and D, five epithelium-free subglottises in basic medium with supplemental TGFbeta3. RESULTS: Groups A and D demonstrated the greatest luminal area expansion. Group A rings demonstrated statistically higher chondrocyte proliferation than Groups B and C and lesser amounts of luminal apoptosis. Groups B and C rings demonstrated the least amount of cell proliferation, and greater luminal apoptosis relative to Group A. Groups A and D rings had similar apoptotic and proliferative results. CONCLUSIONS: Luminal epithelium exerts influence over the cricoid by increasing chondrocyte proliferation and decreasing the relative proportion of luminal chondrocytes that undergo apoptosis. Exogenous TGFbeta3, not TGFbeta1, also increases chondrocyte proliferation within the cricoid and appears to influence apoptosis as well.

Local control of murine subglottis development.

OBJECTIVE: To determine if subglottic development is at least partially under local control and to determine which tissue layer(s) is predominantly responsible. DESIGN: The suglottises of 12 day-3 CD1 mice were grown in whole organ culture. The 12 subglottises were divided into 3 individual groups: +++, -++, and ---. Group+++ had all tissue layers of the subglottis intact: luminal epithelium, cricoid cartilage, inner and outer perichondrium. Group-++ had all layers intact with the exception of luminal epithelium. Group--- had all layers removed (luminal epithelium, inner and outer perichondrium) resulting in cricoid cartilage-only rings. All rings were grown in basic medium without the use of growth factors or serum for 15 days. Measurements of the rings were taken before and after organ culture growth. RESULTS: Group+++ was the only group that experienced growth. Only luminal growth was statistically significant although all rings experienced growth in both the luminal and external diameter. Group-++ did not experience any growth. Group--- lost structural integrity with collapse of the ring and did not experience growth of any dimension of the cartilage. CONCLUSIONS: Growth of the subglottis is under local control but may have additional influences from the outside that were not investigated here. Removal of just the epithelium stunts growth of the entire ring, but preferentially the lumen more so than the external diameter. Removal of all tissue layers around the cricoid cartilage results in a structural collapse of the ring, suggesting that the cartilage in this age group is dependent on surrounding tissues for structural integrity.