The team from Queen Mary University of London (QMUL) used RNA interference to reduce expression of a gene, IFT88, that is involved in cilia elongation. They found that stem cells with shorter cilia did not differentiate into fat cells.
Obesity is characterised by an excess of adipose tissue formed when people consume more calories than they use. The tissue consists of fat cells produced to store energy though a process called adipogenesis.
The ability to stop adipose tissue forming may be a way of preventing the condition according lead researcher Martin Knight, who told us it may be possible to “directly inhibit the cilia transport of the key proteins involved in adipogenesis.”
And the technique has application beyond obesity prevention according to Prof Knight, who explained that because primary cilia are involved in various signalling pathways targeting them may be a way of stopping tumours developing.
“In some cancers, manipulation of hedgehog signalling, which is modulated by primary cilia length, is already used to control tumourogenesis” he said.
Joint disease may also be treatable in this way. Knight said: “Inflammatory signalling, in the context of arthritis and cartilage degradation, also involves changes in cilia length and that manipulation of cilia can prevent this suggesting another potential cilia-therapy.”
He added that: “Currently there are no direct cilia-therapies but we would love to talk to pharmaceutical companies about how our research might facilitate this.”
Knight’s own focus is on the use of nanotechnology implants to control cilia length and cell function. He told us that: “We have shown that tiny grooves on a nanoscale effect stem cell cilia length leading to changes in differentiation.
“Perhaps if we correctly engineer our implant materials we can control the formation of bone or other tissues making these implants more successful.”
Source: Stem Cells
“Adipogenic differentiation of hMSCs is mediated by recruitment of IGF-1R onto the primary cilium associated with elongation.”
Melis T. Dalby, Stephen D. Thorpe, John T. Connelly, J. Paul Chapple and Martin M. Knight.