Control of mucin production by ocular surface epithelial cells

Dartt, Darlene A.

doi:10.1016/j.exer.2003.10.005

Cited by 87 publications

(68 citation statements)

References 60 publications

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“…8 Most conjunctival epithelial cells produce the membrane-spanning mucins Muc1 and Muc4 8 ; goblet cells occupy the conjunctival fornix, resemble intestinal goblet cells in morphology and, like mucus in the GI tract, secrete products that function to lubricate the surface, clear debris, and provide anti-microbial defense. 34 Initial inspection revealed the typical frequency and appearance of goblet cells in Foxq1 sb/sb conjunctivae, and mutant goblet cells stained with both PAS and Alcian blue, similar to controls (Fig. 7B-G); these findings differ from the dramatic loss of PAS signal in Foxq1 sb/sb stomach ( Fig.…”

Section: The Role Of Foxq1 In Muc5ac Gene Regulationcontrasting

confidence: 43%

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Transcription Factor Foxq1 Controls Mucin Gene Expression and Granule Content in Mouse Stomach Surface Mucous Cells

et al. 2008

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Section: The Role Of Foxq1 In Muc5ac Gene Regulationcontrasting

confidence: 43%

“…However, conjunctival goblet cells differ from gastric pit cells, which express only MUC5AC, in that they express multiple mucin glycoproteins. 34 Indeed, immunostaining revealed striking absence of MUC5AC in Foxq1 sb/sb conjunctival goblet cells (Fig. 7H).…”

Section: The Role Of Foxq1 In Muc5ac Gene Regulationmentioning

confidence: 99%

Transcription Factor Foxq1 Controls Mucin Gene Expression and Granule Content in Mouse Stomach Surface Mucous Cells

et al. 2008

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“…Goblet cell hyperplasia results from exposure to high levels of air pollution in the urban population (8) . This is due to chronic exposure to air pollution by human nasal and respiratory mucosal surfaces that are considerably similar to conjunctiva (84,(87)(88)(89) . However, studies in mice exposed to a desiccating environment showed the opposite response.…”

Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 99%

Is dry eye an environmental disease?

Alves¹,

Novaes²,

Morraye³

et al. 2014

Arquivos Brasileiros De Oftalmologia

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Previous studies have revealed that eye contact with either air pollutants or adverse indoor and/or outdoor environmental conditions can affect tear film composition and ocular surface components. These effects are mediated by selective binding of the environmental agents to ocular surface membrane receptors, leading to activation of pro inflammatory signaling pathways. The aim of the current review was to examine the published evidence associated with environmental factors and ocular surface disease and dry eye. Specifically, the reader will appreciate why it is possible to refer to them as mediators of Environmental Dry Eye Disease (EDED), a singular clinical entity inside DED context, directly caused by pollutants and/ or adverse climatic conditions. The indicators and clinical findings are described along with EDE differential diagnosis in its acute and the chronic phases. Based on strong existing evidence of clinical reports and epidemiological observations regarding DED and environmental factors we conclude that there is a straight cause-and-effect relationship between ambient stresses and DED. International standards and web-based tools are described for monitoring worldwide environmental conditions referring localities and populations susceptible to EDED. This information is beneficial to health providers to pinpoint the individuals and predisposed groups afflicted with DED. Such insights may not only improve the understanding and treatment of DED but also help to identify the contributing factors and lower the frequency and progression of EDED. of DED has been studied and confirmed in animal models of human DED (13)(14)(15) . KeywordsAs indicated, a healthy and pain-free ocular surface depends on identifying and eliminating factors that cause ambient humidity, airflow and purity, and temperature to intolerable levels. Such an undertaking is needed to preserve tear film qualities commensurate with ocular surface health. This is essential to sustain sufficient corneal refractive power, visual acuity, and ocular comfort (5,16,17) . A desiccating environment can lead to increase in tear film evaporation and/or decline in its turn over and clearance. These initial events lead to exposure of the ocular surface to hazardous environmental elements that trigger or exacerbate EDED symptoms. Clinical findings have shown that increased numbers of people are affected by EDED because of exposure to environmental factors ( Figure 2).Our purpose herein is to provide a critical appraisal of the clinical and epidemiological evidence indicating that DED is influenced by environmental factors. Secondly, we delineate EDED as a single clinical entity with a unique set of symptoms and clinical findings different from that of either DED or other diseases, such as Sjögren's syndrome, diabetes mellitus or drug induced, allergic conjunctivitis, toxic or irritative conjunctivitis, and actinic keratitis. Moreover, we will describe standard tools used to monitor environmental conditions and discuss their relevance in EDED ep...

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“…Conjunctival goblet cells play a critical role in the physiology of the ocular surface by secreting the soluble, gelforming acidic mucin-5 and other glycoproteins such as peroxidase, trefoil peptides, and defensins into the tear film (18). Because goblet cells do not develop in the Klf4 null colon (33), we examined the development of conjunctival goblet cells in the Klf4CN mice.…”

Section: Conditional Disruption Ofmentioning

confidence: 99%