Building a rheumatology biobank for reliable basic/translational research and precision medicine

Assirelli, Elisa; Naldi, Susanna; Brusi, Veronica; Ciaffi, Jacopo; Lisi, Lucia; Mancarella, Luana; Pignatti, Federica; Pulsatelli, Lia; Faldini, Cesare; Ursini, Francesco; Neri, Simona

doi:10.3389/fmed.2023.1228874

Cited by 1 publication

(1 citation statement)

References 54 publications

(50 reference statements)

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“…Peripheral blood samples from 23 RA patients (12 Female (F)/11 Male (M); mean age 61 ± 16 years), 12 axSpA patients (1 F/11 M; mean age 41 ± 15), 24 PsA patients (12 F/12 M; mean age 54.5 ± 14), along with 13 control subjects with no autoimmune or inflammatory diseases (11 F/2 M; mean age 59.5 ± 19) were obtained from the Rheumatology Biobank of the Istituto Ortopedico Rizzoli [ 39 ]. All patients participating in the Biobank project had provided written informed consent, and the study was approved by the CE-AVEC Ethical Committee (protocol N. 206/2023/Sper/IOR).…”

Section: Methodsmentioning

confidence: 99%

PIM Kinases as Potential Biomarkers and Therapeutic Targets in Inflammatory Arthritides

Assirelli,

Ciaffi,

Scorcu

et al. 2024

IJMS

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The Proviral Integration site for the Moloney murine leukemia virus (PIM)-1 kinase and its family members (PIM-2 and PIM-3) regulate several cellular functions including survival, proliferation, and apoptosis. Recent studies showed their involvement in the pathogenesis of rheumatoid arthritis RA, while no studies are available on psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA). The main objective of this study is to assess the expression of PIM kinases in inflammatory arthritides, their correlation with proinflammatory cytokines, and their variation after treatment with biologic disease-modifying anti-rheumatic drugs or JAK inhibitors. We evaluated PIM-1, -2, and -3 expression at the gene and protein level, respectively, in the peripheral blood mononuclear cells and serum of patients with RA, PsA, axSpA, and healthy individuals (CTR). All the samples showed expression of PIM-1, -2, and -3 kinases both at the gene and protein level. PIM-1 was the most expressed protein, PIM-3 the least. PIM kinase levels differed between controls and disease groups, with reduced PIM-1 protein and increased PIM-3 protein in all disease samples compared to controls. No difference was found in the expression of these molecules between the three different pathologies. PIM levels were not modified after 6 months of therapy. In conclusion, our preliminary data suggest a deregulation of the PIM pathway in inflammatory arthritides. In-depth studies on the role of PIM kinases in this field are warranted.

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Section: Methodsmentioning

confidence: 99%