The size of the primary cilium and acetylated tubulin are modulated during adipocyte differentiation: Analysis of HDAC6 functions in these processes.
Forcioli-Conti N., Estève D., Bouloumié A., Dani C., Peraldi P.
Laboratory Study, published in Biochimie (2015) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Biochimie (2015)
- Country
- France
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 26363102
- DOI
- 10.1016/j.biochi.2015.09.011
Abstract (original English)
The primary cilium is an organelle present in most of the cells of the organism. Ciliopathies, such as the Bardet Biedl and the Alstrom syndromes are associated with obesity. We, and others, have shown that the primary cilium undergoes size modifications during adipocyte differentiation of human adipose stromal cells. We show here that the levels of acetylated α-tubulin, a constituent of the primary cilium, and the expression of HDAC6, the enzyme that deacetylates α-tubulin and is responsible for the loss of the cilium during mitosis, are modulated during adipogenesis. Moreover, during adipocyte differentiation cells that express higher level of HDAC6 are the first to lose their primary cilium. We have investigated the function of HDAC6 on adipocyte differentiation and on the primary cilium. We observe that inhibition of HDAC6 activity leads to a decrease in adipocyte differentiation. This is associated with an inhibition of the initial elongation of the cilium. Interestingly, overexpression of HDAC6 inhibits adipocyte differentiation and blunts the elongation of the primary cilium. In both situations, inhibition of adipocyte differentiation was not associated with an inhibition of the glucocorticoid receptor activity. This indicates that HDAC6 controls adipogenesis through the levels of acetylated α-tubulin. Moreover, we show that although HDAC6 expression increases during adi
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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