Adipose-Derived Mesenchymal Stem Cells Isolated from Patients with Abdominal Aortic Aneurysm Exhibit Senescence Phenomena

• Published in: Oxidative medicine and cellular longevity Vol. 2019; no. 2019; pp. 1 - 12
• Main Authors: Zhang, Yuelin, Li, Xin, Jiang, Guojun, He, Haiwei, Han, Qian, Mao, Mengmeng, Hong, Yimei, Liang, Xiaoting, Zhang, Hao, Huang, Xiaoran, Tao, Wu-Yuan
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2019; Hindawi; Hindawi Limited
• Subjects: Abdomen; Adipocytes; Adipose Tissue - cytology; Age; Aged; Aging; Aneurysms; Aortic Aneurysm, Abdominal - metabolism; Aortic Aneurysm, Abdominal - pathology; Aortic aneurysms; Atherosclerosis; Autophagy; Bone marrow; Cardiovascular disease; Case-Control Studies; Cell Movement; Cell Proliferation; Cellular Senescence; Cytokines; Diabetes; DNA Damage; Female; Genotype & phenotype; Humans; Inflammation; Male; Medical research; Membrane Potential, Mitochondrial; Mesenchymal Stem Cells - cytology; Mesenchymal Stem Cells - metabolism; Microtubule-Associated Proteins - metabolism; Middle Aged; Mitochondria - metabolism; Mitochondria - pathology; Reactive Oxygen Species - metabolism; Senescence; Stem cells
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2019/1305049

Mesenchymal stem cells (MSCs) have shown beneficial effects in the treatment of abdominal aortic aneurysm (AAA). Nonetheless, the biological properties of adipose-derived MSCs (ASCs) from patients with AAA (AAA-ASCs) remain unclear. This study is aimed at investigating the properties of cell phenotype and function of AAA-ASCs compared with ASCs from age-matched healthy donors (H-ASCs). H-ASCs and AAA-ASCs were studied for cell phenotype, differentiation capacity, senescence, and mitochondrial and autophagic functions. Cellular senescence was examined by senescence-associated β-galactosidase (SA-β-gal) staining. Mitochondrial morphology was determined by MitoTracker staining. Despite the similar surface markers of AAA-ASCs and H-ASCs, AAA-ASCs exhibited altered multidifferentiation potential. Compared with H-ASCs, AAA-ASCs displayed enhanced senescence manifested by increased SA-β-gal activity and decreased proliferation and migration ability. Furthermore, AAA-ASCs showed increased mitochondrial fusion, reactive oxygen species (ROS) production, and decreased mitochondrial membrane potential. In addition, AAA-ASCs exhibited decreased autophagy level, upregulation of IL-6 and TNF-α secretion, and downregulation of IL-10 secretion compared with H-ASCs. Nonetheless, treatment of AAA-ASCs with rapamycin (an autophagy activator) dramatically reduced secretion of IL-6 and TNF-α and enhanced secretion of IL-10. In conclusion, our study showed that AAA-ASCs exhibit senescence phenomena and decreased cell function. Understanding the specific alterations in AAA-ASCs will help explore novel strategies to restore cell function for AAA treatment.