Lysophosphatidyl-choline 16: 0 mediates persistent joint pain through Acid-Sensing Ion Channel 3: preclinical and clinical evidences
F Jacquot, S Khoury, B Labrum, K Delanoe, L Pidoux… - BioRxiv, 2021 - biorxiv.org
F Jacquot, S Khoury, B Labrum, K Delanoe, L Pidoux, J Barbier, L Delay, A Bayle…
BioRxiv, 2021•biorxiv.orgRheumatic diseases are often associated to debilitating chronic joint pain, which remains
difficult to treat and requires new therapeutic strategies. Here, we describe increased
content of lysophosphatidyl-choline (LPC) 16: 0 in the knee synovial fluids of two
independent cohorts of patients with painful joint diseases. If LPC16: 0 levels correlated with
pain in patients with osteoarthritis (OA), they do not appear to be the hallmark of a particular
joint disease. We found that intra-articular injections of LPC16: 0 in mouse produce chronic …
difficult to treat and requires new therapeutic strategies. Here, we describe increased
content of lysophosphatidyl-choline (LPC) 16: 0 in the knee synovial fluids of two
independent cohorts of patients with painful joint diseases. If LPC16: 0 levels correlated with
pain in patients with osteoarthritis (OA), they do not appear to be the hallmark of a particular
joint disease. We found that intra-articular injections of LPC16: 0 in mouse produce chronic …
Abstract
Rheumatic diseases are often associated to debilitating chronic joint pain, which remains difficult to treat and requires new therapeutic strategies. Here, we describe increased content of lysophosphatidyl-choline (LPC) 16:0 in the knee synovial fluids of two independent cohorts of patients with painful joint diseases. If LPC16:0 levels correlated with pain in patients with osteoarthritis (OA), they do not appear to be the hallmark of a particular joint disease. We found that intra-articular injections of LPC16:0 in mouse produce chronic pain and anxiety-like behaviors in both males and females with no apparent inflammation, peripheral nerve sprouting and damage, nor bone alterations. LPC16:0-induced persistent pain state is dependent on peripheral Acid-Sensing Ion Channel 3 (ASIC3), ultimately leading to central sensitization. LPC16:0 and ASIC3 thus appear as key players of chronic joint pain with potential implications in OA and possibly across others rheumatic diseases.
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