Pain is relative depending on the person who is receiving it. Given the same stimulus, one person might experience tremendous amounts of pain while others, not so much.
Current studies of pain include mice subjects and although some are very promising, the data that is gathered may not translate to humans. Although this may be the case, some researchers have devised a way to help test pain and its medications.
James Bilsland and Edward Stevens of the Pfizer’s UK-based neuroscience and pain research units and their team have discovered that induced pluripotent stem cells that are harvested from the blood samples of patients with chronic pain disorders, can be utilized to make sensory neurons that will restate the disease phenotype.
In a clinical trial, the researchers were able to test some pain medications on iPSCs that were derived from affected patients. This is done to recapitulate the sensitivity to the drug that is seen in these trials.
Their findings have concluded that stem cells can be used to help study nerve dysfunction. Stevens said that they hope that the method will have wide applications as it pertains to many pain states that can be translated in other areas of therapy.
Paul Knoepfler, a stem cell researcher, also added that their research provides an important foundation in the study of pain thresholds and therapy.
Another stem cell researcher from the Memorial Sloan Kettering Cancer Center, Lorenz Studer, said that the use of the patient’s induced pluripotent stem cells and differentiating them into neurons could provide an avenue to test and help predict a patient’s response to pain and pain medications.
The researchers have extracted iPSCs from the peripheral blood that was given by the four patients that have Erythromelalgia (IEM)- a type of vascular peripheral pain disorder. This was done to test Pfizer’s new pain drug.
The drug acts as an inhibitor and it prohibits the expression of the Nav 1.7 sodium channel, which is responsible for the transmission of pain sensations.
According to the researchers, some people who have this condition have mutations in the SCN9A gene. This, in turn, makes the affected person more hypersensitive to heat pain and stimuli and may experience some extreme episodes of burning pain that is triggered by flames, heat, or other similar stimuli.
A drug that inhibits the Nav 1.7 channel may prevent the spontaneous firing. This suggests that the SCN9A mutations are the likely culprits of inducing the spontaneous firing phenotype. The researchers also said that the neuronal cell lines from patients with IEM were also quite sensitive to moderate heat compared to subjects that do not have IEM.
Although the response of the neurons from the patients may not literally be called “pain”, it may still provide some useful information of the fact.
Even though their research might provide some insight into personalized pain therapies and medications, they understand that their study’s sample size is too small to call it substantial. Hopefully, subsequent studies about this matter would be done as soon as possible.