Periostin Is Essential for the Integrity and Function of the Periodontal Ligament During Occlusal Loading in Mice

Ríos, Héctor F.; Ma, Dedong; Xie, Yixia; Giannobile, William V.; Bonewald, Lynda F.; Conway, Simon; Feng, Jian Q.

doi:10.1902/jop.2008.070624

Cited by 191 publications

(211 citation statements)

References 25 publications

(35 reference statements)

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“…In particular, in PDL cells, Postn, which is among the extracellular matrix adhesion molecules mainly expressed in the bone, periosteum, and PDL tissues (KruzynskaFrejtag et al, 2004;Ma et al, 2011;Rios et al, 2005), was significantly decreased in the M1 PDL in 10-week-old Mkx −/− mice in vivo. In addition, Postn-deficient mice exhibit a phenotype of vertical PDL expansion and alveolar bone resorption in the M1 furcation area (Horiuchi et al, 1999;Rios et al, 2008), suggesting that PDL phenotype in Mkx −/− mice could, in part, be due to the suppression of Postn. If PDL width is expanded because of the absence of Postn and consequently loses its physical strength, it is possible that PDL has a compensating mechanism, and it changes to an osteogenic phenotype.…”

Section: Discussionmentioning

confidence: 99%

Mohawk transcription factor regulates homeostasis of the periodontal ligament

et al. 2016

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The periodontal ligament (PDL), which connects the teeth to the alveolar bone, is essential for periodontal tissue homeostasis. Although the significance of the PDL is recognized, molecular mechanisms underlying PDL function are not well known. We report that mohawk homeobox (Mkx), a tendon-specific transcription factor, regulates PDL homeostasis by preventing its degeneration. Mkx is expressed in the mouse PDL at the age of 10 weeks and expression remained at similar levels at 12 months. In Mkx −/− mice, agedependent expansion of the PDL at the maxillary first molar (M1) furcation area was observed. Transmission electron microscopy (TEM) revealed that Mkx −/− mice presented collagen fibril degeneration in PDL with age, while the collagen fibril diameter gradually increased in Mkx +/+ mice. PDL cells lost their shape in Mkx −/− mice, suggesting changes in PDL properties. Microarray and quantitative polymerase chain reaction (qPCR) analyses of Mkx −/− PDL revealed an increase in osteogenic gene expression and no change in PDL-and inflammatory-related gene expression. Additionally, COL1A1 and COL1A2 were upregulated in Mkxoverexpressing human PDL fibroblasts, whereas osteogenic genes were downregulated. Our results indicate that Mkx prevents PDL degeneration by regulating osteogenesis.

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Section: Discussionmentioning

confidence: 99%

Mohawk transcription factor regulates homeostasis of the periodontal ligament

et al. 2016

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“…Despite lacking an RGD domain, periostin is thought to interact with multiple integrins, including αVβ3, αVβ5, and α6β4, to initiate a variety of biologic effects including cell proliferation, cell migration, epithelial to mesenchymal transformation, modulation of the biomechanical properties of connective tissues, and regeneration of cardiac myocytes after injury (4,8,9). Periostin also binds type 1 collagen to promote fibrillogenesis (10), and periostin-null mice show aberrant type 1 collagen fibrillogenesis in skin and poor integrity of the periodontal ligament in response to mechanical stress (11,12).…”

Section: Mmp-9mentioning

confidence: 99%

Roles of epithelial cell-derived periostin in TGF-β activation, collagen production, and collagen gel elasticity in asthma

Sidhu

Yuan

Innes

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

356

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Periostin is considered to be a matricellular protein with expression typically confined to cells of mesenchymal origin. Here, by using in situ hybridization, we show that periostin is specifically up-regulated in bronchial epithelial cells of asthmatic subjects, and in vitro, we show that periostin protein is basally secreted by airway epithelial cells in response to IL-13 to influence epithelial cell function, epithelial-mesenchymal interactions, and extracellular matrix organization. In primary human bronchial epithelial cells stimulated with periostin and epithelial cells overexpressing periostin, we reveal a function for periostin in stimulating the TGF-β signaling pathway in a mechanism involving matrix metalloproteinases 2 and 9. Furthermore, conditioned medium from the epithelial cells overexpressing periostin caused TGF-β-dependent secretion of type 1 collagen by airway fibroblasts. In addition, mixing recombinant periostin with type 1 collagen in solution caused a dramatic increase in the elastic modulus of the collagen gel, indicating that periostin alters collagen fibrillogenesis or cross-linking and leads to stiffening of the matrix. Epithelial cell-derived periostin in asthma has roles in TGF-β activation and collagen gel elasticity in asthma.airway fibrosis | fibroblasts | epithelial to mesenchymal transition | MMP-2 | MMP-9

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“…9 Various in vitro approaches highlight the importance of geometric control on tissue regeneration/ morphogenesis using a variety of cell types, [10][11][12] but geometric influences on spatiotemporal tissue regeneration and functional healing have had limited assessment in vivo. 3,13 Dental-supportive connective tissue, known as periodontal ligament (PDL), is anchored between mineralized tissue surfaces and plays a key role in the transmission of biomechanical proprioception, 3,13,14 adaptive responses of masticatory cyclic movements, 13 shock absorption of external forces, and tooth movement. These critical functions are related to the orientation of collagenous fiber bundles found in the PDL interface.…”

Section: Introductionmentioning

confidence: 99%