The purpose of this study was to determine the pathogenic changes that occur in myoepithelial cells (MECs) from lacrimal glands of a mouse model of Sjogren’s syndrome. MECs were cultured from lacrimal glands of C57BL/6J (wild type, WT), and thrombospondin 1 null (TSP1) mice, and from mice expressing smooth muscle actin-GFP (SMA-GFP) that labels MECs. MECs were stimulated with cholinergic and α-adrenergic agonists, vasoactive intestinal peptide (VIP), and the purinergic (P)2 agonists, ATP and UTP. Then, intracellular [Ca] ([Ca]) was measured using fura 2 and contraction was observed using live cell imaging. Expression of purinergic receptors was determined by western blot analysis and mRNA expression was analyzed by microarray. The increase in [Ca] with VIP and UTP was significantly smaller in MECs from TSP1 compared to WT mice. Cholinergic agonists, ATP, and UTP stimulated contraction in MECs although contraction of MECs from TSP1 mice was reduced compared to WT mice. The amount of P2Y1, P2Y11, and P2Y13 was significantly decreased in MECs from TSP1 compared to WT mice whereas several extracellular matrix and inflammation genes were upregulated in MECs from TSP1 mice. We conclude that lacrimal gland MEC function is altered by inflammation as the functions regulated by cholinergic agonists, VIP and purinergic receptors are decreased in TSP1 compared to WT mice.
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