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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.
Amezcua-Guerra, Luis M; Sánchez-Muñoz, Fausto; Pichardo-Ontiveros, Edgar; González-Ramírez, Javier; Martínez-Martínez, Laura Aline; Juárez-Vicuña, Yaneli.
Afiliação
  • Amezcua-Guerra LM; Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, and Department of Health Care, Universidad Autónoma Metropolitana-Xochimilco, Mexico City, Mexico.
  • Sánchez-Muñoz F; Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
  • Pichardo-Ontiveros E; Department of Nutrition Physiology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
  • González-Ramírez J; Cell Biology Laboratory, Facultad de Enfermería, Universidad Autónoma de Baja California Campus Mexicali, Mexicali, Baja California, Mexico.
  • Martínez-Martínez LA; Department of Rheumatology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
  • Juárez-Vicuña Y; Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico. yaneli2608@hotmail.com.
Clin Exp Rheumatol ; 40(12): 2275-2282, 2022 Dec.
Article em En | MEDLINE | ID: mdl-36189916
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.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Síndrome de Sjogren / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Clin Exp Rheumatol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: México País de publicação: Itália

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Síndrome de Sjogren / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Clin Exp Rheumatol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: México País de publicação: Itália