Functional expression of the adenosine A1 receptor in rabbit lacrimal gland

Edman, Maria C.; Andersson, Sofia V.; Delbro, Dick; Gierow, J. Peter

doi:10.1016/j.exer.2007.09.014

Cited by 12 publications

(11 citation statements)

References 37 publications

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“…ATP can be converted to ADP, AMP, and adenosine, all which bind to other types of purinergic receptors. It is known that P1 receptors are present in the rabbit lacrimal gland,28 and preliminary evidence indicates that all the P2X receptors with the exception of the P2X5 receptor are present in the rat lacrimal gland. Thus purinergic receptors could play a significant role in the normal function of the lacrimal gland.…”

Section: Discussionmentioning

confidence: 98%

Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland

Hodges¹,

Vrouvlianis²,

Shatos³

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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PURPOSE To characterize the effects of P2X7 purinergic receptors on lacrimal gland function. METHODS P2X7 purinergic receptors were identified by RT-PCR, Western blot analysis, and immunofluorescence techniques. Rat lacrimal gland acini were isolated by collagenase digestion. Acini were incubated with the fluorescent indicator molecule fura 2, and [Ca2+]i was measured by a fluorescence imaging system. Protein secretion was measured with a fluorescence assay system. Activation of ERK 1/2 was determined by Western blot analysis with an antibody against phosphorylated (active) ERK 1/2. RESULTS P2X7 receptors were present in the lacrimal gland by RT-PCR and Western blot analysis. These receptors were located in the membranes of acinar and ductal cells and the cytoplasm of acinar cells. Activation of P2X7 receptors with (benzoylbenzoyl)adenosine 5′-triphosphate increased [Ca2+]i, peroxidase secretion, and ERK 1/2 activation, each of which was inhibited by the P2X7 receptor inhibitors Brilliant Blue G or A 438079. CONCLUSIONS P2X7 purinergic receptors are present in rat lacrimal gland and when stimulated increase [Ca2+]i, protein secretion, and ERK 1/2 activation.

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Section: Discussionmentioning

confidence: 98%

Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland

Hodges¹,

Vrouvlianis²,

Shatos³

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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“…In humans, the VIP receptor 1 was identified on the basolateral membrane of the acinar cells, whereas the VIP receptor 2 was localized to the myoepithelial cells. Application of VIP to isolated rabbit acinar cells or to the isolated porcine lacrimal gland increases protein secretion [237,260–263]. When both muscarinic and adrenergic receptors were blocked, application of a VIP receptor antagonist produced a small reduction in protein secretion evoked by electrical stimulation of the nerves supplying the isolated porcine lacrimal gland [261].…”

Section: Neural Regulation Of Tear Productionmentioning

confidence: 99%

TFOS DEWS II pain and sensation report

et al. 2017

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Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglia mechano- and polymodal nociceptor neurons while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of Meibonian gland secretion or mucins release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.

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“…3B). In a previous study, 21 lower concentrations of Cch plus another agonist showed a synergistic secretory effect in rabbit lacrimal gland cells. In our model of monkey lacrimal acinar cells, 0.1 lM each of Cch plus lacritin did not show any synergistic effect (data not shown).…”

Section: Lacritin-induced Secretion Of Tear Proteins From Cultured Momentioning

confidence: 99%

Lacritin-Induced Secretion of Tear Proteins From Cultured Monkey Lacrimal Acinar Cells

Fujii

Morimoto-Tochigi

Walkup

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. During inflammation of the ocular surface, increased proinflammatory cytokines depress tear protein secretion, suggesting that a decline in lacrimal cell function contributes to dry eye. Lacritin, a glycoprotein secreted from lacrimal acinar cells, may function as an autocrine factor to stimulate tear protein secretion. The purpose of the present experiment was to investigate lacritin-induced protein secretion in normal and cytokine-pretreated (inflammation model) monkey acinar cells.METHODS. Acinar cells from monkey lacrimal glands were cultured with or without tumor necrosis factor alpha (TNF-a) plus interferon gamma (IFN-c). Protein secretion was induced by lacritin or carbachol (Cch, positive control). Proteins were detected and identified by immunoblotting and immunocytochemistry. Intracellular Ca 2þ was measured with the fluorophore Calcium-4, and cell damage was determined by LDH leakage into the culture medium. RESULTS. In cultured monkey acinar cells, lacritin stimulated tear protein secretion in normal cells without elevating intracellular Ca 2þ. In contrast, Cch elevated intracellular Ca 2þ and release of tear proteins. This contrast suggested an alternate, calcium-independent mechanism for lacritin-induced protein secretion. TNF-a plus IFN-c caused LDH leakage from sensitive human corneal epithelial cells, but even higher doses of TNF-a plus IFN-c did not cause LDH leakage from monkey acinar cells, suggesting a higher tolerance against these cytokines. In cytokine-treated acinar cells, lacritin stimulated protein secretion as much as that in normal cells. In contrast, Cch-induced elevation of Ca 2þ and release of proteins were depressed by cytokines.CONCLUSIONS. Lacritin might be a useful biotechnology-based treatment agent against ocular surface diseases where endogenous lacritin is inadequate.

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Functional expression of the adenosine A1 receptor in rabbit lacrimal gland

Cited by 12 publications

References 37 publications

Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland

Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland

TFOS DEWS II pain and sensation report

Lacritin-Induced Secretion of Tear Proteins From Cultured Monkey Lacrimal Acinar Cells

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Functional expression of the adenosine A1 receptor in rabbit lacrimal gland

Cited by 12 publications

References 37 publications

Characterization of P2X7Purinergic Receptors and Their Function in Rat Lacrimal Gland

Characterization of P2X7Purinergic Receptors and Their Function in Rat Lacrimal Gland

TFOS DEWS II pain and sensation report

Lacritin-Induced Secretion of Tear Proteins From Cultured Monkey Lacrimal Acinar Cells

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Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland

Characterization of P2X₇Purinergic Receptors and Their Function in Rat Lacrimal Gland