Filamin B and CD13 Are Components of Senescent Secretomes That May Be Involved in Primary (Stress Induced) and Paracrine Senescence of Mesenchymal Stromal Cells
1Department of Medical, Surgical, Neurological, Metabolic Sciences, and Aging; 2nd Division of Neurology, Center for Rare Diseases and InterUniversity Center for Research in Neurosciences, University of Campania “Luigi Vanvitelli,” Naples, Italy
2Genome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey
3Research Institute on Terrestrial Ecosystems, National Research Council, Naples, Italy
4Department of Experimental Medicine, Campania University “Luigi Vanvitelli,” Naples, Italy
5Department of Biology, Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA, USA
J Clin Pract Res 2019; 41(2): 135-140 DOI: 10.14744/etd.2019.37974
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Objective: In the present study we aim to evaluate whether some of the proteins previously identified in the secretome of senescent bone marrow (BM)- and adipose (A)-mesenchymal stromal cells (MSCs) could be involved in regulation of senescence phenomena.
Materials and Methods: Among the identified proteins, we selected Filamin B (FLNB) and Aminopeptidase N (CD13) that were exclusively found in the secretome of senescent cells. We silenced their mRNA expression in BM-MSCs by means of RNA interference technology and induced acute senescence by hydrogen peroxide treatment. Our goal was to evaluate if FLNB or CD13 silencing may affect onset of senescence.
Results: Our preliminary data showed that CD13 protein could be a key factor involved in the regulation and determination of both primary and paracrine induced senescence in human BM-MSCs. On the other hand, Filamin B seems not to be involved in the determination of primary senescence whereas its presence could be part of the mechanism that regulates the senescence induction in human BM-MSCs by paracrine signaling.
Conclusion: Our study provides a useful base for identifying the complex extracellular protein networks involved in the regulation of MSC cellular senescence.