Iron overload inhibits calcification and differentiation of ATDC5
J Biochem. 2011 Oct 11.
Ohno T, Hashimoto N, Mitsui K, Nishimura H, Hagiwara H.
SourceDepartment of Biological Sciences, Tokyo Institute of
Technology, 4259 Nagatsuta-cho, Midori-ku,Yokohama 226-8501, Japan.

There is a little information about the effects of iron overload on
cartilage metabolism.
In the present study, we examined the effects of excess iron on the
differentiation and mineralization of cultured chondrocytes, ATDC5
cells. We used ferric ammonium citrate (FAC) as a ferric ion donor and
desferrioxamine (DFO) as a ferric ion chelator.
Neither chemical affected the production of proteoglycan, a marker of
an early stage of ATDC5 differentiation.
In contrast, FAC inhibited the deposition of calcium, a late-stage
event in chondrocyte differentiation, by ATDC5 cells in a dose-
dependent manner, and DFO accelerated it.
Energy dispersive X-ray spectroscopy/scanning electron microscope
analysis revealed that the levels of iron and calcium in cells treated
with FAC were increased and decreased, respectively.
Furthermore, FAC inhibited the expression of matrix metalloproteinase
13 mRNA, another marker of late-stage chondrocyte differentiation.
In addition, we found that the heavy and light chains of ferritin were
expressed specifically at a late stage of ATDC5 differentiation, and
the levels of both proteins were enhanced by the addition of iron.
These results suggest that iron overload might give rise to osteopenia
and arthritis by inhibiting chondrocyte differentiation and


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