TY  - JOUR
A1  - Ritter, Andreas Hans
A1  - Friemel, Alexandra
A1  - Kreis, Nina-Naomi
A1  - Hoock, Samira Catharina
A1  - Roth, Susanne
A1  - Kielland-Kaisen, Ulrikke
A1  - Brüggmann, Dörthe
A1  - Solbach, Christine
A1  - Louwen, Frank
A1  - Yuan, Juping
T1  - Primary cilia are dysfunctional in obese adipose-derived mesenchymal stem cells
T2  - Stem cell reports
N2  - Adipose-derived mesenchymal stem cells (ASCs) have crucial functions, but their roles in obesity are not well defined. We show here that ASCs from obese individuals have defective primary cilia, which are shortened and unable to properly respond to stimuli. Impaired cilia compromise ASC functionalities. Exposure to obesity-related hypoxia and cytokines shortens cilia of lean ASCs. Like obese ASCs, lean ASCs treated with interleukin-6 are deficient in the Hedgehog pathway, and their differentiation capability is associated with increased ciliary disassembly genes like AURKA. Interestingly, inhibition of Aurora A or its downstream target the histone deacetylase 6 rescues the cilium length and function of obese ASCs. This work highlights a mechanism whereby defective cilia render ASCs dysfunctional, resulting in diseased adipose tissue. Impaired cilia in ASCs may be a key event in the pathogenesis of obesity, and its correction might provide an alternative strategy for combating obesity and its associated diseases.
KW  - adipose-derived mesenchymal stem cells
KW  - primary cilium
KW  - obesity
KW  - Aurora A
KW  - IL-6
KW  - TNF-α
KW  - hedgehog signaling
Y1  - 2018
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/46386
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-463866
SN  - 2213-6711
N1  - This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
VL  - 10
IS  - 2
SP  - 583
EP  - 599
PB  - Cell Press ; Elsevier
CY  - Maryland Heights, MO ; [New York, NY]
ER  -