RT Journal Article
T1 Adipogenic Impairment of Adipose Tissue-Derived Mesenchymal Stem Cells in Subjects With Metabolic Syndrome: Possible Protective Role of FGF2.
A1 Oliva-Olivera, Wilfredo
A1 Coin-Aragüez, Leticia
A1 Lhamyani, Said
A1 Clemente-Postigo, Mercedes
A1 Torres, Juan Alcaide
A1 Bernal-Lopez, Maria Rosa
A1 El-Bekay, Rajaa
A1 Tinahones, Francisco Jose
K1 Mesenchymal Stem Cells
K1 Metabolic Syndrome
K1 Middle Aged
K1 Obesity, Morbid
K1 Perilipin-1
K1 RNA, Messenger
AB The decreased expansion capacity of adipose tissue plays a crucial role in the onset of disorders associated with metabolic syndrome. The aim of this study was to examine the state of adipose tissue-derived mesenchymal stem cells (ASCs) from obese subjects with different metabolic profiles. This was a 2-year study to enroll subjects who underwent bariatric surgery or cholecystectomy. University Hospital. Patients who underwent either bariatric surgery (20 morbidly obese) or cholecystectomy (40 subjects) participated in the study. ASCs were obtained from both visceral and subcutaneous adipose tissue. Adipogenic, fibrotic gene expression was quantified by quantitative polymerase chain reaction; Smad7 and fibroblast growth factor 2 were quantified by western blotting and enzyme-linked immunosorbent assay, respectively. The susceptibility of ASCs to apoptosis, their population doubling time, and their clonogenic potential were evaluated. The worsening metabolic profile of the patients was accompanied by a decrease in the intrinsic levels of adipogenic gene expression, reduced proliferation rate, clonogenic potential, and exportation of fibroblast growth factor 2 to the cell surface of the ASCs derived from both tissues. In addition, the ASCs from patients without metabolic syndrome showed differences in susceptibility to apoptosis and expression of TGFβ-signaling inhibitory protein Smad7 with respect to the ASCs from patients with metabolic syndrome. Our results suggest that the decrease in adipogenic-gene mRNA and clonogenic potential, as well as the accumulation of fibrotic proteins with metabolic alterations, could be a relevant mechanism controlling the number and size of neogenerated adipocytes and involved in alteration of adipose-tissue expansion.
PB Oxford University Press
YR 2016
FD 2016-12-14
LK http://hdl.handle.net/10668/10678
UL http://hdl.handle.net/10668/10678
LA en
NO Oliva-Olivera W, Coín-Aragüez L, Lhamyani S, Clemente-Postigo M, Torres JA, Bernal-López MR, et al. Adipogenic Impairment of Adipose Tissue-Derived Mesenchymal Stem Cells in Subjects With Metabolic Syndrome: Possible Protective Role of FGF2. J Clin Endocrinol Metab. 2017 Feb 1;102(2):478-487
NO This work was cofunded by the European Union through the European Regional Development Fund and supported by grants from the Ministry of Economy and Competitiveness, ISCII (Grants PI13/02628, PI12/02355, FIS PI14/00696, and PI12/01373), and the Ministry of Economy and Knowledge (Grants PI-CTS-08181/2011, CTS-7895/2011, and CTS-656). R. E.-B. and M. B.-L. are supported by a fellowship from the ISCIII “Miguel Servet II” (CP13/00041) and “Miguel Servet I” (CP15/00028).
DS RISalud
RD Apr 19, 2025