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Copyright (c) 2024 Khalid Mohany, Mansour Alsharidah, Mona Elsafadi, Osamah Al Rugaie, Amer Mahmood, Khalid A. Al-Regaiey, Khaleel I. Alyahya, Abdel-Moneim Hafez Abdel-Moneim , Abir El Sadik, Mohammad Abumaree
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Mesenchymal stem cells treated with Interleukin-1 beta for mediation of an inflammatory response in human tissues
Corresponding Author(s) : Mansour Alsharidah
Cellular and Molecular Biology,
Vol. 70 No. 10: Issue 10
Abstract
The present study examined the functional activities of the human bone marrow mesenchymal stem cells (hBM-MSCs) under the effects of various concentrations of the inflammatory mediator interleukin 1 beta (IL-1β). The effects of IL-1β on the functional properties of hBM-MSCs were measured using functional assays (adhesion, proliferation, and migration). hBM-MSCs expressions of colony-stimulating factors 1 and 2 (CSF1, CSF2), C-C chemokine receptor type 2 (CCR2), C-X-C chemokine receptor type 1 and 3 (CXCL1, CXCL3), were examined using real-time polymerase chain reaction (RT‒PCR). The pro-inflammatory cytokine IL-1β did not disrupt hBM-MSCs adhesion, but it improved proliferation and migration only up to 50 ng/ml. However, in response to 100 ng/ml IL-1β, cell growth, proliferation, and migration were reduced significantly. The expression of CSF1, CCR2, CXCL3, and IL-1β genes increased with the increase in the concentration of IL-1β. CSF2 and CXCL1 gene expression increased in the 50ng/ml group compared with the 10ng/ml group to be higher than the control group in the 100ng/ml IL-1β group which might facilitate the differentiation, and homing of MSCs to the site of injury and augment their activities in the inflamed microenvironment. The study corroborates the advantages of prior stimulation of mesenchymal stem cells (MSCs) with the cytokine IL-1β, demonstrating an upregulation of key chemokines and cytokines. This upregulation potentially enhances MSCs' ability to differentiate and migrate to injury sites, while also augmenting their functional role within an inflamed microenvironment, thereby amplifying their therapeutic potential.
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