Nada Lukkahatai1, Brian Walitt2, Alexandra Espina3, Dan Wang3, Leorey N Saligan4. 1. School of Nursing, University of Nevada, Las Vegas, NV, USA National Institute of Nursing Research (NINR), National Institutes of Health (NIH), Bethesda, MD, USA. 2. National Institute of Nursing Research (NINR), National Institutes of Health (NIH), Bethesda, MD, USA Section of Rheumatology, Washington Hospital Center, Washington, DC, USA. 3. National Institute of Nursing Research (NINR), National Institutes of Health (NIH), Bethesda, MD, USA. 4. National Institute of Nursing Research (NINR), National Institutes of Health (NIH), Bethesda, MD, USA saliganl@mail.nih.gov.
Abstract
BACKGROUND: Fibromyalgia syndrome (FMS), a chronic musculoskeletal condition characterized by diffuse pain, fatigue, sleep impairment, and cognitive dysfunction, is associated with significant functional disability. Its underlying biological mechanisms are unknown. This study investigated differentially expressed genes between women with FMS and healthy volunteers. METHODS: Women who met the 1990 or 2010 American College of Rheumatology fibromyalgia criteria were compared to age- and race-matched pain-free healthy women. Peripheral blood samples were collected, and a full genome microarray gene expression analysis was performed. One-way analysis of variance was used to identify differentially expressed genes using the filtering criterion of 1% false discovery rate. Analysis of canonical pathways associated with these genes was performed. Confirmatory quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay verified microarray results. Independent t-tests compared gene and protein expression between groups. RESULT: Participants were 54 women with FMS and 25 controls. Expression arrays from a subset of women with FMS (n = 29) and controls (n = 20) showed upregulation of 12 genes (>1.8-fold change, p < .05) in the FMS sample. Differentially expressed genes were related to B-cell development, primary immunodeficiency signaling, and mitotic roles of polo-like kinase. CENPK and HSP90AA1 were the most differentially expressed genes (p < .01). CONCLUSION: Activity of interrelated pathways related to immune response, and homeostasis appears to be relevant to the experience of FMS. Replication and exploration of the relationship between gene expression and symptom severity will help determine clinical relevance of these findings.
BACKGROUND:Fibromyalgia syndrome (FMS), a chronic musculoskeletal condition characterized by diffuse pain, fatigue, sleep impairment, and cognitive dysfunction, is associated with significant functional disability. Its underlying biological mechanisms are unknown. This study investigated differentially expressed genes between women with FMS and healthy volunteers. METHODS:Women who met the 1990 or 2010 American College of Rheumatology fibromyalgia criteria were compared to age- and race-matched pain-free healthy women. Peripheral blood samples were collected, and a full genome microarray gene expression analysis was performed. One-way analysis of variance was used to identify differentially expressed genes using the filtering criterion of 1% false discovery rate. Analysis of canonical pathways associated with these genes was performed. Confirmatory quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay verified microarray results. Independent t-tests compared gene and protein expression between groups. RESULT: Participants were 54 women with FMS and 25 controls. Expression arrays from a subset of women with FMS (n = 29) and controls (n = 20) showed upregulation of 12 genes (>1.8-fold change, p < .05) in the FMS sample. Differentially expressed genes were related to B-cell development, primary immunodeficiency signaling, and mitotic roles of polo-like kinase. CENPK and HSP90AA1 were the most differentially expressed genes (p < .01). CONCLUSION: Activity of interrelated pathways related to immune response, and homeostasis appears to be relevant to the experience of FMS. Replication and exploration of the relationship between gene expression and symptom severity will help determine clinical relevance of these findings.
Authors: Andrea T White; Alan R Light; Ronald W Hughen; Timothy A Vanhaitsma; Kathleen C Light Journal: Psychosom Med Date: 2011-12-30 Impact factor: 4.312
Authors: Jonathan R Kerr; Robert Petty; Beverley Burke; John Gough; David Fear; Lindsey I Sinclair; Derek L Mattey; Selwyn C M Richards; Jane Montgomery; Don A Baldwin; Paul Kellam; Tim J Harrison; George E Griffin; Janice Main; Derek Enlander; David J Nutt; Stephen T Holgate Journal: J Infect Dis Date: 2008-04-15 Impact factor: 5.226
Authors: Jaime C Branco; Bernard Bannwarth; Inmaculada Failde; Jordi Abello Carbonell; Francis Blotman; Michael Spaeth; Fernando Saraiva; Francesca Nacci; Eric Thomas; Jean-Paul Caubère; Katell Le Lay; Charles Taieb; Marco Matucci-Cerinic Journal: Semin Arthritis Rheum Date: 2009-02-27 Impact factor: 5.532
Authors: Kim D Jones; Terri Gelbart; Thomas C Whisenant; Jill Waalen; Tony S Mondala; David N Iklé; Daniel R Salomon; Robert M Bennett; Sunil M Kurian Journal: Clin Exp Rheumatol Date: 2016-02-12 Impact factor: 4.473
Authors: Vivek Verma; Gillian L Drury; Marc Parisien; Ayşe N Özdağ Acarli; Tho-Alfakar Al-Aubodah; Anastasia Nijnik; Xia Wen; Nicol Tugarinov; Maria Verner; Richie Klares; Alexander Linton; Emerson Krock; Carlos E Morado Urbina; Bendik Winsvold; Lars G Fritsche; Egil A Fors; Ciriaco Piccirillo; Arkady Khoutorsky; Camilla I Svensson; Mary A Fitzcharles; Pablo M Ingelmo; Nicole F Bernard; Franck P Dupuy; Nurcan Üçeyler; Claudia Sommer; Irah L King; Carolina B Meloto; Luda Diatchenko Journal: Pain Date: 2021-09-24 Impact factor: 7.926
Authors: Mari A Griffioen; Joseph Glutting; Robert V O'Toole; Angela R Starkweather; Debra Lyon; Susan G Dorsey; Cynthia L Renn Journal: Nurs Res Date: 2020 Mar/Apr Impact factor: 2.381
Authors: Nada Lukkahatai; Brian Walitt; Enrique J Deandrés-Galiana; Juan Luis Fernández-Martínez; Leorey N Saligan Journal: J Pain Res Date: 2018-11-21 Impact factor: 3.133