Activating distinct signalling pathways may help protect bone mass

Lead researcher

Natalie A Sims

Main finding

In a mouse model of spontaneous osteopenia caused by hyperactivation of STAT1/3 signalling downstream of gp130 (gp130Y757F/Y757F), STAT1 deletion rescued the osteopenic phenotype of these mice, indicating a beneficial effect of promoting STAT3 signalling over STAT1 downstream of gp130 in this low bone mass condition, and this may have therapeutic value.


Centre for Innate Immunity & Infectious Diseases

Research group

Cancer and Immune Signalling Laboratory


Emma C Walker, Rachelle W Johnson, Yifang Hu, Holly J Brennan, Ingrid J Poulton, Jian-Guo Zhang, Brendan J Jenkins, Gordon K Smyth, Nicos A Nicola

Journal and article title

J Biol Chem

Murine Oncostatin M acts via Leukemia Inhibitory Factor Receptor to phosphorylate STAT3 but not STAT1, an effect that protects bone mass

Most surprising

This study identified unique downstream signalling pathways of mOSM:mLIFR compared to hOSM:mLIFR and mLIF:mLIFR, and determined mechanisms by which such distinct signalling pathways could be activated.

Future implications

These findings could have potential therapeutic value in the future at designing reagents to combat low bone mass conditions.

Disease/health impact