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Interferon-alpha regulates expression of lncRNA MALAT1 and interferon-stimulated genes, as well as chemokine production, in primary Sjögren's syndrome
L.M. Amezcua-Guerra1, F. Sánchez-Muñoz2, E. Pichardo-Ontiveros3, J. González-Ramírez4, L.A. Martínez-Martínez5, Y. Juárez-Vicuña6
- Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, and Department of Health Care, Universidad Autónoma Metropolitana-Xochimilco, Mexico City, Mexico.
- Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
- Department of Nutrition Physiology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
- Cell Biology Laboratory, Facultad de Enfermería, Universidad Autónoma de Baja California Campus Mexicali, Mexicali, Baja California, Mexico.
- Department of Rheumatology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
- Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico. yaneli2608@hotmail.com
CER15830
2022 Vol.40, N°12
PI 2275, PF 2282
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PMID: 36189916 [PubMed]
Received: 06/05/2022
Accepted : 28/07/2022
In Press: 26/09/2022
Published: 20/12/2022
Abstract
OBJECTIVES:
This study aimed to explore the contribution of interferon-alpha (IFN-α) to MALAT1 expression in primary Sjögren’s syndrome (pSS).
METHODS:
Peripheral blood mononuclear cells (PBMC) from pSS patients and healthy blood donors were stimulated with recombinant human IFN-α, and the expression levels of MALAT1 and several interferon-stimulated genes (ISGs) were measured by RT-PCR, while supernatant levels of interferon-regulated chemokines were measured using multiplex cytokine immunobead assay.
RESULTS:
In this work, we found that MALAT1 expression levels were increased in IFN-α-stimulated PBMC from pSS patients and healthy controls. As expected, ISG expression levels and interferon-regulated chemokine secretion levels were higher after IFN-α stimulation. However, the fold-change values for ISG15, Ly6E, OAS1, and OASL expression levels were higher in cells from pSS patients than in controls. Similarly, PBMC from pSS patients produced higher concentrations of chemokines than those from healthy controls after IFN-α stimulation.
CONCLUSIONS:
Our data provide insights into the abnormal IFN-α-mediated regulation of the lncRNA MALAT1 in pSS. Based on an unusually high capacity of PBMC to express ISG and to produce interferon-responsive chemokines, it is likely that targeted therapies to block these molecules may be of benefit to patients with pSS.
