Aquaporin gene therapy corrects Sjögren’s syndrome phenotype in mice

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dc.contributor.authorLai, Zhennan
dc.contributor.authorYin, Hongen
dc.contributor.authorCabrera-Pérez, Javier
dc.contributor.authorDiniz, Maria Cambraia Guimaro
dc.contributor.authorAfione, Sandra
dc.contributor.authorMichael, Drew G.
dc.contributor.authorGlenton, Patricia
dc.contributor.authorPatel, Ankur
dc.contributor.authorSwaim, William D.
dc.contributor.authorZheng, Changyu
dc.contributor.authorNguyen, Cuong Q.
dc.contributor.authorNyberg, Fred
dc.contributor.authorChiorini, John A.
dc.date.accessioned2022-10-31T15:02:19Z
dc.date.available2022-10-31T15:02:19Z
dc.date.issued2016-05-02
dc.description.abstractPrimary Sjögren’s syndrome (pSS) is a chronic autoimmune diseasethat is estimated to affect 35 million people worldwide. Currently, noeffective treatments exist for Sjögren’s syndrome, and there is alimited understanding of the physiological mechanisms associatedwith xerostomia and hyposalivation. The present work revealed thataquaporin 5 expression, a water channel critical for salivary glandfluid secretion, is regulated by bone morphogenetic protein 6. In-creased expression of this cytokine is strongly associated with themost common symptom of primary Sjögren’s syndrome, the loss ofsalivary gland function. This finding led us to develop a therapy inthe treatment of Sjögren’s syndrome by increasing the water perme-ability of the gland to restore saliva flow. Our study demonstratesthat the targeted increase of gland permeability not only resulted inthe restoration of secretory gland function but also resolved thehallmark salivary gland inflammation and systemic inflammation as-sociated with disease. Secretory function also increased in the lacri-mal gland, suggesting this local therapy could treat the systemicsymptoms associated with primary Sjögren’ssyndrome.en_US
dc.description.sponsorshipWe thank the staff of the Sjögren’s syndrome clinic atthe NIDCR, NIH for providing salivary gland tissue and patient diagnosis; mem-bers of the NIDCR animal facility fortheir ongoing assistance in the animalmodel maintenance; and patients with Sjögren’s syndrome and HVs for con-tributing to this study. This study was supported by Swedish Medical ResearchGrant 9549 (to Z.L. and F.N.), an NIDCR, NIH intramural research grant (to J.A.C.),and NIDCR, NIH extramural research Grants DE023433 and DE018958(to P.G. and to C.Q.N.). We thank Drs. James Melvin, Shmuel Muallem, InduAmbudkar, and Sarah Knox for comments during review and discussion of thismanuscript and the NIH Fellows Editorial Board for editorial assistance.en_US
dc.description.urihttps://www.pnas.org/doi/abs/10.1073/pnas.1601992113?cookieSet=1en_US
dc.format.extent6 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m2j3qf-ocgp
dc.identifier.citationLai, Zhennan et al. "Aquaporin gene therapy corrects Sjögren’s syndrome phenotype in mice." Proceedings of the National Academy of Sciences 113, no. 20 ( May 2, 2016): 5694-5699. https://doi.org/10.1073/pnas.1601992113en_US
dc.identifier.urihttps://doi.org/10.1073/pnas.1601992113
dc.identifier.urihttp://hdl.handle.net/11603/26243
dc.language.isoen_USen_US
dc.publisherPNASen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Office of the Dean of the College of Natural and Mathematical Sciences
dc.rightsThis work was written as part of one of the author's official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.en_US
dc.rightsPublic Domain Mark 1.0*
dc.rights.urihttp://creativecommons.org/publicdomain/mark/1.0/*
dc.titleAquaporin gene therapy corrects Sjögren’s syndrome phenotype in miceen_US
dc.typeTexten_US
dcterms.creatorhttps://orcid.org/0000-0002-2633-9710en_US

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