Gene regulating severity of tissue damage in rheumatoid arthritis identified.


Rheumatoid arthritis (RA) is the most common inflammatory of the types of arthritis affecting around 1% of the population.  RA is an autoimmune disease that causes inflammation, pain, stiffness and damage to the joints of the feet, hips, knees, and hands.  One of the biggest difficulties with treating the condition is early diagnosis. With early diagnosis and aggressive treatment, it is possible to reduce the damage to the joints caused by RA. Deciding the most appropriate treatment for each patient at the earliest possible stage is central to effectively tackling the condition.

Now, researchers from the University College Dublin and the University of Sheffield have identified a new gene, C5orf30, which encodes the 206-aa protein; which in turn regulates the severity of tissue damage caused by rheumatoid arthritis (RA).  The team state that rheumatoid arthritis patients most likely to suffer the severest effects of the condition can now be identified early and fast-tracked to the more aggressive treatments available.  The study is published in the journal PNAS.

Previous studies estimate that 30% of patients with rheumatoid arthritis are unable to work within 10 years of onset of the condition. It affects more women than men, and often more severely. It is also most common between the ages of 40 and 70, however, it can affect people of any age including children.  Although there is no cure for RA, new effective drugs are increasingly available to treat the disease and prevent deformed joints. Self-management of the condition by patients, including exercise, is also known to reduce pain and resulting disability.

The current study analysed DNA samples and biopsy samples from joints of over 1,000 Rheumatoid arthritis patients in the United Kingdom and Ireland. The data findings identified a genetic marker, C5orf30, that could be used to identify those RA patients who require more aggressive treatments or precision medicine.

The researchers surmise that treatments for arthritis have improved enormously over the last number of years. They go on to add that thirty years ago, rheumatologists’ waiting rooms were filled with people in wheelchairs. The lab conclude that in the present the outlook for a person diagnosed with arthritis in 2015 is much brighter than it used to be.  For the future the lab state that these exciting findings will prompt them to further explore the role of this highly conserved protein and its significance in human health and disease.

Source:  The University of Sheffield

C5orf30KD following in vivo administration was assessed in mouse tissue 72 h after injection of the siRNA complex. DBA/1 mice were injected i.v. with siRNA to C5orf30 and NTC (n=3). After 3 d, the mice were culled and organs and joints assessed for knockdown by using qRT-PCR. The results show mRNA concentrations of C5orf30KD compared with the NTC-treated mice.  This bone erosion was quantified by counting the average number of objects per slice on the 2D micro-CT images of the calcaneus, using image analysis software.  C5orf30 is a negative regulator of tissue damage in rheumatoid arthritis.  Wilson et al 2015.

C5orf30KD following in vivo administration was assessed in mouse tissue 72 h after injection of the siRNA complex. DBA/1 mice were injected i.v. with siRNA to C5orf30 and NTC (n=3). After 3 d, the mice were culled and organs and joints assessed for knockdown by using qRT-PCR. The results show mRNA
concentrations of C5orf30KD compared with the NTC-treated mice. This bone erosion was quantified by counting the average number of objects per slice on the 2D micro-CT images of the calcaneus, using image analysis software. C5orf30 is a negative regulator of tissue damage in rheumatoid arthritis. Wilson et al 2015.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s