Researchers at the NYU Pain Research Center have found a new receptor for nerve growth factor that plays an important role in pain signaling, even though it does not signal on its own, according to a study published in the Journal of Clinical Investigation.
New York UniversityDec 6 2024 The findings hold promise for finding new treatments for arthritis and other forms of inflammatory and cancer pain, without the side effects that led recent therapies to fail in clinical trials.
Nerve growth factor is a protein that stimulates the development of neurons. It is also a powerful driver of pain in animals and humans, and is released by cells from injured or diseased tissue. To transmit pain signals, nerve growth factor binds to a receptor called tropomyosin receptor kinase A, or TrkA.
To determine this, they observed that nerve growth factor has a stretch of amino acids that is known to allow other proteins to bind to NPR1. NRP1 was also expressed in the same cells at the nerve growth factor receptor TrkA. Related StoriesIn further cellular studies, the researchers discovered two mechanisms that explain the NRP1's role in pain. First, when binding to nerve growth factor, NRP1 increases the local concentration of nerve growth factor that is presented to TrkA, the signaling receptor. In addition, NRP1 was found to be a molecular chaperone, or a protein that aids in the trafficking of other proteins in the cell-;in this case, TrkA.
A "springboard" for pain treatments Given the newfound role of NRP1 in nerve growth factor pain signaling, the researchers envision several ways that this knowledge can be used to redeploy existing therapies to treat pain and create new ones. The researchers are also harnessing their new understanding of the pain signaling complex, determining the sites at which nerve growth factor, TrkA, and NRP1 interact, and generating peptides that disrupt them. In the Journal of Clinical Investigation study, the researchers created one such peptide that blocked the ability of nerve growth factor to interact with NRP1, which stopped pain in cellular studies.
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