ArticleClinical and experimental immunology2001
Acetylcholine-evoked calcium mobilization and ion channel activation in human labial gland acinar cells from patients with primary Sjögren's syndrome.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- Primary Sjögren's syndrome: new perspectives on salivary gland epithelial cells.European journal of medical research · 2024Review
- Identification of new candidate drugs for primary Sjögren's syndrome using a drug repurposing transcriptomic approach.Rheumatology (Oxford, England) · 2023Article
- Salivary gland proteins alterations in the diabetic milieu.Journal of molecular histology · 2021Review
- IL-17 drives salivary gland dysfunction via inhibiting TRPC1-mediated calcium movement in Sjögren's syndrome.Clinical & translational immunology · 2021Article
- Cytokine/Chemokine/Growth Factor Profiles Contribute to Understanding the Pathogenesis of the Salivary Gland Dysfunction in Euthyroid Hashimoto's Thyroiditis Patients.Mediators of inflammation · 2021Article
- Understanding the Complexity of Sjögren's Syndrome: Remarkable Progress in Elucidating NF-κB Mechanisms.Journal of clinical medicine · 2020Review
- B cell dysregulation in primary Sjögren's syndrome: A review.The Japanese dental science review · 2019Review
- Update on Pathogenesis of Sjogren's Syndrome.Current rheumatology reviews · 2017Review
- cAMP-dependent recruitment of acidic organelles for Ca2+ signaling in the salivary gland.American journal of physiology. Cell physiology · 2016Article
- Detection of autoantibodies against aquaporin-5 in the sera of patients with primary Sjögren's syndrome.Immunologic research · 2016Article
- Younger patients with primary Sjögren's syndrome are more likely to have salivary IgG anti-muscarinic acetylcholine receptor type 3 antibodies.Clinical rheumatology · 2016Article
- IP3R deficit underlies loss of salivary fluid secretion in Sjögren's Syndrome.Scientific reports · 2015Article
- Functional Histology of Salivary Gland Pleomorphic Adenoma: An Appraisal.Head and neck pathology · 2015Review
- Dysfunction of lacrimal and salivary glands in Sjögren's syndrome: nonimmunologic injury in preinflammatory phase and mouse model.Journal of biomedicine & biotechnology · 2011Review
- Activation of the alternative NFκB pathway improves disease symptoms in a model of Sjogren's syndrome.PloS one · 2011Article
- Current concepts: mouse models of Sjögren's syndrome.Journal of biomedicine & biotechnology · 2011Review
- Unraveling the pathophysiology of Sjogren syndrome-associated dry eye disease.The ocular surface · 2009Review
- Sjögren's syndrome--study of autoantigens and autoantibodies.Clinical reviews in allergy & immunology · 2007Review
- Rat salivary gland ligation causes reversible secretory hypofunction.Acta physiologica (Oxford, England) · 2007Article
- Effect of inflammation on lacrimal gland function.Experimental eye research · 2006Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence has indicated that the salivary gland dysfunction associated with Sjögren's syndrome (SjS) is not necessarily due to immune-mediated destruction of acinar tissue. SjS sufferers may possess substantial reserves of acinar tissue but nevertheless be incapable of maintaining salivary flow rates in the normal range. We have investigated the ability of isolated labial gland acinar cells from SjS patients to fluid secrete by measuring agonist-evoked changes in intracellular Ca(2+) ([Ca(2+)](i)) using fura-2 microfluorimetry and activation of K(+) and Cl(-) channels using the patch-clamp whole cell technique. We can confirm that stimulation with a super-maximal dose of acetylcholine (ACh) increased [Ca(2+)]i equally in both control acinar cells and those derived from SjS patients. However, at submaximal concentrations, the dose-response curve for ACh was shifted to the right by approximately one order of magnitude in acinar cells from SjS patients compared to control acinar cells. Patch-clamp measurements consistent with the presence of Ca(2+)-activated K(+) and Cl(-) conductances were obtained from both control acinar cells and those obtained from SjS patients. Dose-dependent activation of the ion channels by acetylcholine was also right-shifted in acinar cells from SjS patients compared to control cells. Our data show that labial gland acinar cells from SjS patients were capable of responding to agonist stimulation by mobilizing [Ca(2+)](i) and activating K(+) and Cl(-) channels consistent with the requirements of fluid secretion. However, the persistent loss of sensitivity to ACh observed in from SjS patients may account for the lack of saliva production observed in these patients in vivo.
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