caa a22 4500 606235469 CHVBK 20210128101242.0 cr unu---uuuuu 210128e20151001xx s 000 0 eng 10.1007/s11010-015-2487-y doi (NATIONALLICENCE)springer-10.1007/s11010-015-2487-y Angiotensin II directly impairs adipogenic differentiation of human preadipose cells [Elektronische Daten] [Marisol Palominos, Natalia Dünner, Martin Wabitsch, Cecilia Rojas] Angiotensin II reduces adipogenic differentiation of preadipose cells present in the stroma-vascular fraction of human adipose tissue, which also includes several cell types. Because of the ability of non-adipose lineage cells in the stroma-vascular fraction to respond to angiotensin II, it is not possible to unequivocally ascribe the anti-adipogenic response to a direct effect of this hormone on preadipose cells. Therefore, we used the human Simpson-Golabi-Behmel syndrome (SGBS) preadipocyte cell strain to investigate the consequences of angiotensin II treatment on adipogenic differentiation under serum-free conditions, by assessing expression of typical adipocyte markers perilipin and fatty acid-binding protein 4 (FABP4), at the transcript and protein level. Reverse transcription-polymerase chain reaction showed that perilipin and FABP4 transcripts were, respectively, reduced to 0.33±0.07 (P<0.05) and 0.41±0.19-fold (P<0.05) in SGBS cells induced to adipogenic differentiation in the presence of angiotensin II. Western Blot analysis corroborated reduction of the corresponding proteins to 0.23±0.21 (P<0.01) and 0.46±0.30-fold (P<0.01) the respective controls without angiotensin II. Angiotensin II also impaired morphological changes associated with early adipogenesis. Hence, we demonstrated that angiotensin II is able to directly reduce adipogenic differentiation of SGBS preadipose cells. Springer Science+Business Media New York, 2015 Angiotensin II nationallicence Adipogenic differentiation nationallicence Anti-adipogenesis nationallicence Adipocyte number regulation nationallicence SGBS preadipose cells nationallicence Palominos Marisol Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut Dünner Natalia Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut Wabitsch Martin Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany aut Rojas Cecilia Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 408/1-2(2015-10-01), 115-122 0300-8177 408:1-2<115 2015 408 11010 https://doi.org/10.1007/s11010-015-2487-y text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2487-y text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Palominos Marisol Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut NATIONALLICENCE 700 1- Dünner Natalia Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut NATIONALLICENCE 700 1- Wabitsch Martin Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany aut NATIONALLICENCE 700 1- Rojas Cecilia Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Clasificador 7 Correo 7, Santiago, Chile aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 408/1-2(2015-10-01), 115-122 0300-8177 408:1-2<115 2015 408 11010