ArticleAmerican journal of physiology. Cell physiology2006
Effects of alpha1D-adrenergic receptors on shedding of biologically active EGF in freshly isolated lacrimal gland epithelial cells.
Article in American journal of physiology. Cell physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 39 citations in OpenAlex.
- A gatekeeper sympathetic control of lacrimal tear secretion and dry eye onset through the NA-Adra1a-Ucp2 pathway.Nature communications · 2025Article
- Review
- Adrenoceptors in the Eye - Physiological and Pathophysiological Relevance.Handbook of experimental pharmacology · 2024Review
- Phenylephrine increases tear cathepsin S secretion in healthy murine lacrimal gland acinar cells through an alternative secretory pathway.Experimental eye research · 2021Article
- ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress.Frontiers in cell and developmental biology · 2021Review
- Alpha-Adrenergic Agonists Stimulate Fluid Secretion in Lacrimal Gland Ducts.Investigative ophthalmology & visual science · 2020Article
- Resolvin D1, but not resolvin E1, transactivates the epidermal growth factor receptor to increase intracellular calcium and glycoconjugate secretion in rat and human conjunctival goblet cells.Experimental eye research · 2019Article
- Activation of the EGF Receptor by Histamine Receptor Subtypes Stimulates Mucin Secretion in Conjunctival Goblet Cells.Investigative ophthalmology & visual science · 2018Article
- Alteration in nerves and neurotransmitter stimulation of lacrimal gland secretion in the TSP-1Mucosal immunology · 2018Article
- Enhanced Tearing by Electrical Stimulation of the Anterior Ethmoid Nerve.Investigative ophthalmology & visual science · 2017Article
- Signaling Pathways of Purinergic Receptors and Their Interactions with Cholinergic and Adrenergic Pathways in the Lacrimal Gland.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2016Review
- Cross-talk between alpha1D-adrenoceptors and transient receptor potential vanilloid type 1 triggers prostate cancer cell proliferation.BMC cancer · 2014Article
- Signaling pathways used by EGF to stimulate conjunctival goblet cell secretion.Experimental eye research · 2012Article
- Genome-wide genetic associations with IFNγ response to smallpox vaccine.Human genetics · 2012Article
- The relationship between the MMP system, adrenoceptors and phosphoprotein phosphatases.British journal of pharmacology · 2012Review
- Interaction of alpha1D-adrenergic and P2X(7) receptors in the rat lacrimal gland and the effect on intracellular [Ca2+] and protein secretion.Investigative ophthalmology & visual science · 2011Article
- alpha1-Adrenergic receptors regulate neurogenesis and gliogenesis.Molecular pharmacology · 2009Article
- Neural regulation of lacrimal gland secretory processes: relevance in dry eye diseases.Progress in retinal and eye research · 2009Review
- The aging lacrimal gland: changes in structure and function.The ocular surface · 2008Review
- ERK/p44p42 mitogen-activated protein kinase mediates EGF-stimulated proliferation of conjunctival goblet cells in culture.Investigative ophthalmology & visual science · 2008Article
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7 authors at 4 institutions in 2 countries.
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Abstract
Transactivation of EGF receptors by G protein-coupled receptors is a well-known phenomenon. This process involves the ectodomain shedding of growth factors in the EGF family by matrix metalloproteinases. However, many of these studies employ transformed and/or cultured cells that overexpress labeled growth factors. In addition, few studies have shown that EGF itself is the growth factor that is shed and is responsible for transactivation of the EGF receptor. In this study, we show that freshly isolated, nontransformed lacrimal gland acini express two of the three known alpha(1)-adrenergic receptors (ARs), namely, alpha(1B)- and alpha(1D)-ARs. Alpha(1D)-ARs mediate phenylephrine (an alpha(1)-adrenergic agonist)-induced protein secretion and activation of p42/p44 MAPK, because the alpha(1D)-AR inhibitor BMY-7378, but not the alpha(1A)-AR inhibitor 5-methylurapidil, inhibits these processes. Activation of p42/p44 MAPK occurs through transactivation of the EGF receptor, which is inhibited by the matrix metalloproteinase ADAM17 inhibitor TAPI-1. In addition, phenylephrine caused the shedding of EGF from freshly isolated acini into the buffer. Incubation of freshly isolated cells with conditioned buffer from cells treated with phenylephrine resulted in activation of the EGF receptor and p42/p44 MAPK. The EGF receptor inhibitor AG1478 and an EGF-neutralizing antibody blocked this activation of p42/p44 MAPK. We conclude that in freshly isolated lacrimal gland acini, alpha(1)-adrenergic agonists activate the alpha(1D)-AR to stimulate protein secretion and the ectodomain shedding of EGF to transactivate the EGF receptor, potentially via ADAM17, which activates p42/p44 MAPK to negatively modulate protein secretion.
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