Filamin B and CD13 Are Components of Senescent Secretomes That May Be Involved in Primary (Stress Induced) and Paracrine Senescence of Mesenchymal Stromal Cells

Conclusion: Our study provides a useful base for identifying the complex extracellular protein networks involved in the regulation of MSC cellular senescence.

📌 3 Key Takeaways

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Objective & Hypothesis: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.

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Key Findings & Data: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.

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Conclusion & Impact:Conclusion: Our study provides a useful base for identifying the complex extracellular protein networks involved in the regulation of MSC cellular senescence.

🔬Design:Research Article

📍Scope:Comprehensive Sample

⚙️Variables:Domain Parameters

Özet

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.

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Cite This Article

SQUILLARO, T., ÖZCAN, S., ALESSIO, N., ACAR, M. B., BERNARDO, G. D., MELONE, M. A. B., PELUSO, G., GALDERİSİ, U. (2019). Filamin B and CD13 Are Components of Senescent Secretomes That May Be Involved in Primary (Stress Induced) and Paracrine Senescence of Mesenchymal Stromal Cells. Erciyes Medical Journal, Cilt: 41 - Sayı: 2, 135–140. https://ajindex.com/articles/161669

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References (2)

Venkatachalam G, Surana U, Clément MV. Replication stress-induced endogenous DNA damage drivescellular senescence induced by a sublethal oxidative stress. Nucleic Acids Res 2017;45:10564–82. [CrossRef] Özcan S, Alessio N, Acar MB, Toprak G, Gönen ZB, Peluso G, et al. Myeloma cells can corrupt senescent mesenchymal stromal cellsand impair their anti-tumor activity. Oncotarget 2015;6:39482–92. [CrossRef] Özcan S, Alessio N, Acar MB, Mert E, Omerli F, Peluso G, et al. Unbiased analysis of senescence associated secretory phenotype(SASP) to identify common components following differentgenotoxic stresses. Aging (Albany NY) 2016;8:1316–29. [CrossRef] Alessio N, Özcan S, Tatsumi K, Murat A, Peluso G, Dezawa M, et al. The secretome of MUSE cells contains factors that may play a rolein regulation of stemness, apoptosis and immunomodulation. Cell Cycle 2017;16:33–44. [CrossRef] Serrano M. Senescence helps regeneration. Dev Cell 2014;31:671–2.
Capasso S, Alessio N, Squillaro T, Di Bernardo G, Melone MA, Cipollaro M, et al. Changes in autophagy, proteasome activity and metabolism to determine a specific signature for acute and chronic senescentmesenchymal stromal cells. Oncotarget 2015;6:39457–68. [CrossRef] Fumagalli M, d’Adda di Fagagna F. SASPense and DDRama in cancer and ageing. Nat Cell Biol 2009;11:921–3. [CrossRef] Coppé JP, Desprez PY, Krtolica A, Campisi J. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu Rev Pathol 2010;5:99–118. [CrossRef] Kuilman T, Peeper DS. Senescence-messaging secretome: SMS-ing cellular stress. Nat Rev Cancer 2009;9:81–94. [CrossRef] Jori FP, Napolitano MA, Melone MA, Cipollaro M, Cascino A, Giordano A, et al. Role of RB and RB2/P130 genes in marrow stromal stem cellsplasticity. J Cell Physiol 2004;200:201–12. [CrossRef] Galderisi U, Giordano A. The gap between the physiological and therapeutic roles of mesenchymal stem cells. Med Res Rev 2014;34:1100– 26. [CrossRef] Squillaro T, Peluso G, Galderisi U. Clinical Trials With Mesenchymal Stem Cells: An Update. Cell Transplant 2016;25:829–48. [CrossRef] Ranganath SH, Levy O, Inamdar MS, Karp JM. Harnessing the mesenchymal stem cell secretome for the treatment of cardiovascular dis ease. Cell Stem Cell 2012;10:244–58. [CrossRef] Lunyak VV, Amaro-Ortiz A, Gaur M. Mesenchymal Stem Cells Secretory Responses: SenescenceMessaging Secretome and Immunomodulation Perspective. Front Genet 2017;8:220. [CrossRef] Dominici M, Le Blanc K, Mueller I, Slaper-Cortenb