Integrin adhesion in regulation of lacrimal gland acinar cell secretion

Andersson, Sofia V.; Gierow, J. Peter

doi:10.1016/j.exer.2006.02.006

Cited by 7 publications

(8 citation statements)

References 54 publications

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“…Interestingly, our data confirm these observations, showing that the significantly down-regulated expression of major ECM protein genes was even more pronounced in tissues isolated from 6 week old NOD mice, when compared to LGs from 18 week old animals, suggesting that the process of ECM degradation is closely coupled to the onset of the disease. The important role of extracellular matrix in modulating lacrimal acinar secretory responses has been established in a number of studies (Chen et al 1998; Laurie et al, 1996; Andersson et al, 2006), so it is perhaps unsurprising that disruption of these interactions might rapidly be accompanied by functional quiescence.…”

Section: Discussionmentioning

confidence: 99%

Lymphocytic infiltration leads to degradation of lacrimal gland extracellular matrix structures in NOD mice exhibiting a Sjögren's syndrome-like exocrinopathy

Schenke‐Layland¹,

Xie

Magnusson

et al. 2010

Experimental Eye Research

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We previously reported that lacrimal glands (LGs) of male non-obese diabetic (NOD) mice, an established mouse model of autoimmune inflammatory LG disease that displays many features of human LGs in patients afflicted with Sjögren’s syndrome (SjS), exhibit significant degradation of extracellular matrix (ECM) structures as well as increased expression of matrix metalloproteinases (MMPs). The purpose of the current study was to expand the spectrum of proteases identified, to identify their probable origin as well as to clarify the contribution of these changes to disease pathogenesis. We explored in depth the changes in ECM structures and ECM protease expression at the onset of disease (6 weeks) versus late stage disease (18 weeks) in male NOD mouse LGs, relative to age-matched male NOD-scid, a severely immunocompromised congenic strain, and healthy BALB/c mice. LG tissues were examined using routine histological, immunohistochemical, Western Blot and gene expression analyses, as well as with novel multiphoton imaging technologies. We further characterized the profile of infiltrating immune cells under each condition using flow cytometry. Our results show that the initial infiltrating cells at 6 weeks of age are responsible for increased MMP and cathepsin H expression and therefore initiate the LG ECM degradation in NOD mice. More importantly, NOD-scid mice exhibited normal LG ECM structures, indicating the lymphocytes seen in the LGs of NOD mice are responsible for the degradation of the LG ECM. The disease-related remodeling of LG ECM structures may play a crucial role in altering the acinar signaling environment, disrupting the signaling scaffolds within the cells, which are required to mobilize the exocytotic trafficking machinery, ultimately leading to a loss of LG function in patients afflicted with SjS.

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Section: Discussionmentioning

confidence: 99%

Lymphocytic infiltration leads to degradation of lacrimal gland extracellular matrix structures in NOD mice exhibiting a Sjögren's syndrome-like exocrinopathy

Schenke‐Layland¹,

Xie

Magnusson

et al. 2010

Experimental Eye Research

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“…Receptors (integrins) located in the basolateral plasma membrane interact with basal lamina proteins and thereby trigger a variety of cellular responses, including secretory processes 27 28. Thus, if these membrane receptors are surrounded by a modified environment, changes in the interaction between proteins of both compartments could alter receptor functionality, even under circumstances where ligands or agonists are still present 27 28. Previous studies have reported variations in the organisation and expression of several laminins and nidogens in acini of patients with Sjögren syndrome.…”

Section: Discussionmentioning

confidence: 99%

Reduced sulfation of muc5b is linked to xerostomia in patients with Sjogren syndrome

Alliende

Kwon

Brito

et al. 2008

Annals of the Rheumatic Diseases

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“…Intraarterial or intraperitoneal systemic administration of acetylcholine, pilocarpine, or other cholinergic agonists stimulates lacrimal gland protein and fluid secretion measured from the cannulated lacrimal gland excretory duct of anesthetized rabbits (Dartt and Botelho 1979; Dartt, Knox et al 1980; Dartt, Moller et al 1981; Ubels, Foley et al 1986; Rismondo and Ubels 1987; Rismondo, Ubels et al 1988; Ubels, Rismondo et al 1989). Incubation of lacrimal gland pieces or acini with the cholinergic agonist carbachol stimulates protein secretion measured by peroxidase secretion from rat and mouse (Herzog, Sies et al 1976; Dartt, Baker et al 1984; Dartt, Donowitz et al 1984), and β-hexosaminidase secretion from rabbit (Andersson Exp Eye Res 1081-1088-2006). …”

Section: Neural Stimulation Of Lacrimal Gland Secretion- Cholinergmentioning

confidence: 99%

Neural regulation of lacrimal gland secretory processes: Relevance in dry eye diseases

Dartt

2009

Progress in Retinal and Eye Research

396

370

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The lacrimal gland is the major contributor to the aqueous layer of the tear film which consists of water, electrolytes and proteins. The amount and composition of this layer is critical for the health, maintenance, and protection of the cells of the cornea and conjunctiva (the ocular surface). Small changes in the concentration of tear electrolytes have been correlated with dry eye syndrome. While the mechanisms of secretion of water, electrolytes and proteins from the lacrimal gland differ, all three are under tight neural control. This allows for a rapid response to meet the needs of the cells of the ocular surface in response to environmental conditions. The neural response consists of the activation of the afferent sensory nerves in the cornea and conjunctiva to stimulate efferent parasympathetic and sympathetic nerves that innervate the lacrimal gland. Neurotransmitters are released from the stimulated parasympathetic and sympathetic nerves that cause secretion of water, electrolytes, and proteins from the lacrimal gland and onto the ocular surface. This review focuses on the neural regulation of lacrimal gland secretion under normal and dry eye conditions.

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Integrin adhesion in regulation of lacrimal gland acinar cell secretion

Cited by 7 publications

References 54 publications

Lymphocytic infiltration leads to degradation of lacrimal gland extracellular matrix structures in NOD mice exhibiting a Sjögren's syndrome-like exocrinopathy

Lymphocytic infiltration leads to degradation of lacrimal gland extracellular matrix structures in NOD mice exhibiting a Sjögren's syndrome-like exocrinopathy

Reduced sulfation of muc5b is linked to xerostomia in patients with Sjogren syndrome

Neural regulation of lacrimal gland secretory processes: Relevance in dry eye diseases

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