Adalimumab changes the expression profile of selected BCL-2 family genes.
BCL2 family
drug resistance
psoriatic arthritis
Journal
Dermatologic therapy
ISSN: 1529-8019
Titre abrégé: Dermatol Ther
Pays: United States
ID NLM: 9700070
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
16
10
2019
revised:
11
01
2020
accepted:
11
02
2020
pubmed:
19
2
2020
medline:
15
5
2021
entrez:
19
2
2020
Statut:
ppublish
Résumé
Biological drugs are an alternative to treatment of psoriasis and psoriatic arthritis. Adalimumab is a representative of the anti-TNF group. The underlying of this disease is a cellular homeostasis disorder-apoptosis. Many proteins are involved in the apoptosis induction pathways, including those from the BCL-2 family. The aim of the study was to perform a transcriptional analysis of the genes coding selected proteins from the BCL-2 family in patients treated with adalimumab therapy, and to determine the direction of these changes. The test materials were peripheral blood mononuclear cells. The cells were obtained from 20 patients with psoriatic arthritis who were being treated with adalimumab (study group) and 20 healthy volunteers (control). The gene expression profile was determined using the real-time quantitative reverse transcription polymerase chain reaction technique. Statistically significant changes were observed in the expression level of the BNIP3, BNIP3L, and BCL2L1 genes (p < .05) during a 24-month observation of therapy. We indicated that adalimumab therapy has an impact on the expression of the analyzed genes, which may constitute a new class of molecular markers for assessing the effectiveness of a therapy. It appears that the BNIP3L gene could be used as a potential diagnostic marker of psoriasis.
Substances chimiques
Proto-Oncogene Proteins c-bcl-2
0
Tumor Necrosis Factor-alpha
0
Adalimumab
FYS6T7F842
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13277Subventions
Organisme : Medical University of Silesia in Katowice, Poland
ID : KNW-2-I10/D/9/N
Pays : International
Informations de copyright
© 2020 Wiley Periodicals LLC.
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