Basonuclin in murine corneal and lens epithelia correlates with cellular maturation and proliferative ability

Tseng, Hung; Matsuzaki, Kyoichi; Lavker, Robert M.

doi:10.1046/j.1432-0436.1999.6540221.x

Cited by 23 publications

(23 citation statements)

References 21 publications

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“…7A). Consistent with previous data (Tseng et al, 1999), we found that proliferation rates of basal CECs (assessed as percentage of BrdU-positive CECs at the cornea center and periphery) were high (16-18%) at P9 but decreased to 7-9% at P13 in both control and mutant mice (Fig. 7B).…”

Section: Decreased Activity Of Notch Signaling Precedes Proliferationsupporting

confidence: 92%

“…During postnatal mouse development, CE proliferation rates steadily increase during the first week of life peaking around P7-10 and beginning to decline prior to the eyelid opening at P12-15 (Tseng et al, 1999). Interestingly, it was reported that Notch activity, assessed by N1ICD staining, becomes detectable in basal and suprabasal CECs around P10 and appears more intense at P90 (Djalilian et al, 2008).…”

Section: Decreased Activity Of Notch Signaling Precedes Proliferationmentioning

confidence: 99%

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

et al. 2016

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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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Section: Decreased Activity Of Notch Signaling Precedes Proliferationsupporting

confidence: 92%

Section: Decreased Activity Of Notch Signaling Precedes Proliferationmentioning

confidence: 99%

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

et al. 2016

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“…This notion is suggested in the mouse or rat corneal epithelium where some corneal basal epithelial cells still retain SC function postnatally before SCs become sequestered to the limbal area [74,[117][118][119]. Therefore, if these findings hold well not just for rodents but also humans, future studies are needed to determine whether postnatal stimuli such as eye opening and exposure to the air via the tear film play a role in facilitating the maturation of the limbal SC niche.…”

Section: When and How Does Limbal Stem Cell Niche Form During Morphogmentioning

confidence: 99%

Niche regulation of corneal epithelial stem cells at the limbus

et al. 2007

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Among all adult somatic stem cells, those of the corneal epithelium are unique in their exclusive location in a defined limbal structure termed Palisades of Vogt. As a result, surgical engraftment of limbal epithelial stem cells with or without ex vivo expansion has long been practiced to restore sights in patients inflicted with limbal stem cell deficiency. Nevertheless, compared to other stem cell examples, relatively little is known about the limbal niche, which is believed to play a pivotal role in regulating self-renewal and fate decision of limbal epithelial stem cells. This review summarizes relevant literature and formulates several key questions to guide future research into better understanding of the pathogenesis of limbal stem cell deficiency and further improvement of the tissue engineering of the corneal epithelium by focusing on the limbal niche.

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“…In early postnatal life, proliferating cells are found throughout the basal corneal epithelium (Tseng et al, 1999;Yew et al, 2001). However, as shown in Figure 1, the mass of the adult corneal epithelium is maintained by a population of stem-like cells in the basal limbal region (limbal stem cells) that continue to cycle slowly throughout life, unless stimulated to proliferate more rapidly by corneal injury (Davanger and Evensen, 1971;Cotsarelis et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Clonal analysis of patterns of growth, stem cell activity, and cell movement during the development and maintenance of the murine corneal epithelium

Collinson

Morris

Reid

et al. 2002

Developmental Dynamics

139

228

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Basonuclin in murine corneal and lens epithelia correlates with cellular maturation and proliferative ability

Cited by 23 publications

References 21 publications

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

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

Niche regulation of corneal epithelial stem cells at the limbus

Clonal analysis of patterns of growth, stem cell activity, and cell movement during the development and maintenance of the murine corneal epithelium

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