Notch Signaling in Skeletal Stem Cells

Chen, Shan; Lee, Brendan; Bae, Yangjin

doi:10.1007/s00223-013-9773-z

Cited by 39 publications

(32 citation statements)

References 85 publications

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“…These cells could theoretically be activated to participate in repair and regeneration of the enthesis. To explore whether this small cell population had progenitor cell characteristics, immunostaining was performed for Notch1, an important stem cell regulator involved in skeletogenesis (Chen et al, 2014;Mead and Yutzey, 2012). In the mature enthesis, staining of Notch1 was limited to the small number of remaining Gli1+ cells (Fig.…”

Section: Gli1 Expression Is Activated During Early Stages To Regeneramentioning

confidence: 99%

Enthesis regeneration: a role for Gli1+ progenitor cells

2017

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The tendon enthesis originates from a specific pool of hedgehogactive Gli1+ progenitor cells that differentiate and produce mineralized fibrocartilage. The current study investigated the regenerative capacity of this cell population by comparing the responses of early postnatal and mature entheses to injury. Lineage tracing studies demonstrated that the original Gli1+ cell population had the capacity to heal immature entheses after injury, but this capacity was lost after the cells differentiated into mature fibrochondrocytes. To further examine the involvement of Gli1+ cells and hedgehog signaling in enthesis healing, Gli1 expression was examined via lineage tracing approaches and the effect of Smo deletion was examined in the injured entheses. Immature injured entheses retained high levels of Gli1 expression, a marker of hedgehog activation, consistent with non-injured controls. In contrast, injured mature entheses had few Gli1+ cells early in the healing process, with limited recovery of the cell population later in the healing process. These results suggest that the presence of activated hedgehog signaling in enthesis cells early in the healing process may enhance healing of enthesis injuries by mimicking developmental processes.

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Section: Gli1 Expression Is Activated During Early Stages To Regeneramentioning

confidence: 99%

Enthesis regeneration: a role for Gli1+ progenitor cells

2017

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“…Mouse genetic deletions and human genetic mutations in Notch signaling are associated with a variety of defects in patterning, axial skeleton development, and skeletal diseases [83, 84]. Notch signaling is important for chondrocyte hypertrophy in part via regulating Sox9 expression [83] [85].…”

Section: Notch Signalingmentioning

confidence: 99%

Signaling pathways regulating cartilage growth plate formation and activity

Samsa

Zhou

2017

Seminars in Cell & Developmental Biology

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The growth plate is a highly specialized and dynamic cartilage structure that serves many essential functions in skeleton patterning, growth and endochondral ossification in developing vertebrates. Major signaling pathways initiated by classical morphogens and by other systemic and tissuespecific factors are intimately involved in key aspects of growth plate development. As a corollary of these essential functions, disturbances in these pathways due to mutations or environmental factors lead to severe skeleton disorders. Here, we review these pathways and the most recent progress made in understanding their roles in chondrocyte differentiation in growth plate development and activity. Furthermore, we discuss newly uncovered pathways involved in growth plate formation, including mTOR, the circadian clock, and the COP9 signalosome.

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“…In addition, it was shown that disruption of IFT components diminishes Notch activity leading to compromised skin differentiation and barrier function (Ezratty et al, 2011). Notch signaling plays a key role in proliferation and differentiation of several tissues (Chen et al, 2014;Guentchev and McKay, 2006). Activation of the pathway occurs through the interaction of Notch ligands of the Delta-like and Jagged families with the receptors of the Notch family (Notch1-4).…”

Section: Introductionmentioning

confidence: 99%

Primary cilia maintain corneal epithelial homeostasis by regulation of the Notch signaling pathway

Grisanti¹,

Revenkova²,

Gordon³

et al. 2016

Journal of Cell Science

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Primary cilia have been linked to signaling pathways involved in cell proliferation, cell motility and cell polarity. Defects in ciliary function result in developmental abnormalities and multiple ciliopathies. Patients affected by severe ciliopathies, such as Meckel syndrome, present several ocular surface disease conditions of unclear pathogenesis. Here, we show that primary cilia are predominantly present on basal cells of the mouse corneal epithelium (CE) throughout development and in the adult. Conditional ablation of cilia in the CE leads to an increase in proliferation and vertical migration of basal corneal epithelial cells (CECs). A consequent increase in cell density of suprabasal layers results in a thicker than normal CE. Surprisingly, in cilia-deficient CE, cilia-mediated signaling pathways, including Hh and Wnt pathways, were not affected but the intensity of Notch signaling was severely diminished. Although Notch1 and Notch2 receptors were expressed normally, nuclear Notch1 intracellular domain (N1ICD) expression was severely reduced. Postnatal development analysis revealed that in ciliadeficient CECs downregulation of the Notch pathway precedes cell proliferation defects. Thus, we have uncovered a function of the primary cilium in maintaining homeostasis of the CE by balancing proliferation and vertical migration of basal CECs through modulation of Notch signaling.

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Notch Signaling in Skeletal Stem Cells

Cited by 39 publications

References 85 publications

Enthesis regeneration: a role for Gli1+ progenitor cells

Enthesis regeneration: a role for Gli1+ progenitor cells

Signaling pathways regulating cartilage growth plate formation and activity

Primary cilia maintain corneal epithelial homeostasis by regulation of the Notch signaling pathway

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