β-NGF and β-NGF receptor upregulation in blood and synovial fluid in osteoarthritis

Montagnoli, Claudia; Tiribuzi, Roberto; Crispoltoni, Lucia; Pistilli, Alessandra; Stabile, Anna Maria; Manfreda, Francesco; Placella, Giacomo; Rende, Mario; Cerulli, Giuliano Giorgio

doi:10.1515/hsz-2016-0280

Cited by 43 publications

(37 citation statements)

References 40 publications

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“…Increased NGF levels have been reported in inflammatory conditions such as rheumatoid arthritis, spondyloarthritis, and osteoarthritis . We previously evaluated Ngf mRNA expression in the acute phase of injury and revealed that expression was increased 1 day after disc injury in mice, as was also observed in the present study.…”

Section: Discussionsupporting

confidence: 88%

Changes in Nerve Growth Factor Expression and Macrophage Phenotype Following Intervertebral Disc Injury in Mice

Nakawaki

Uchida

Miyagi

et al. 2019

Journal Orthopaedic Research

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Nerve growth factor (NGF) is increased in intervertebral discs (IVDs) after disc injury and anti-NGF therapy improves low back pain in humans. Furthermore, M1 and M2 macrophage subtypes play a role in degenerative IVD injury. We examined M1 and M2 macrophage markers and NGF and cytokine expression in IVD-derived cells from control and IVD-injured mice for 28 days following injury. Ngf messenger RNA (mRNA) expression was increased 1 day after injury in injured compared with control mice, and persisted for up to 28 days. Flow cytometric analysis demonstrated that the proportion of F4/80+ CD11b+ cells was significantly increased from 1 day after injury for up to 28 days in injured compared to control mice. mRNA expression of M1 macrophage markers Tnfa, Il1b, and Nos2 was significantly increased 1 day after injury in injured compared to control mice, before gradually decreasing. At 28 days, no significant difference was observed in M1 markers. The M2a marker, Ym1, was significantly increased 1 day after injury in injured compared with control mice, while M2a and M2c markers Tgfb and Cd206 were significantly increased 7, 14, and 28 days after injury. Tumor necrosis factor α (TNF-α) and transforming growth factor β (TGF-β) stimulated Ngf mRNA and NGF protein expression in IVD cells. Our results suggest that TNF-α and TGF-β may stimulate NGF production under inflammatory and non-inflammatory conditions following IVD injury. As TNF-α and TGF-β are produced by M1 and M2 macrophages, further investigations are needed to reveal the role of macrophages in NGF expression following IVD injury. Our results may aid in developing treatments for IVD-related LBP pathology.

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Section: Discussionsupporting

confidence: 88%

Changes in Nerve Growth Factor Expression and Macrophage Phenotype Following Intervertebral Disc Injury in Mice

Nakawaki

Uchida

Miyagi

et al. 2019

Journal Orthopaedic Research

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“… 40 Thus, NGF concentrations are increased in chronic pain conditions such as interstitial cystitis, prostatitis, arthritis, pancreatitis, chronic headaches, cancer pain, diabetic neuropathy, and noncancer pain, suggesting that NGF-mediated signaling is an ongoing and active process in chronic nociceptive and neuropathic pain states. 12 , 41 – 51 Given the evidence that NGF plays an important role in driving skeletal pain, one important data set that we still do not have is what specific sets of cells in the intact bone express NGF, TrkA, or p75. 4 , 32 , 33 , 52 …”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localization of nerve growth factor, tropomyosin receptor kinase A, and p75 in the bone and articular cartilage of the mouse femur

et al. 2017

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Sequestration of nerve growth factor (NGF) significantly attenuates skeletal pain in both animals and humans. However, relatively little is known about the specific cell types that express NGF or its cognate receptors tropomyosin receptor kinase A (TrkA) and p75 in the intact bone and articular cartilage. In the present study, antibodies raised against NGF, TrkA, and p75 (also known as CD271) were used to explore the expression of these antigens in the non-decalcified young mouse femur. In general, all three antigens displayed a remarkably restricted expression in bone and cartilage with less than 2% of all DAPI+ cells in the femur displaying expression of any one of the three antigens. Robust NGF immunoreactivity was found in mostly CD-31− blood vessel-associated cells, a small subset of CD-31+ endothelial cells, an unidentified group of cells located at the subchondral bone/articular cartilage interface, and a few isolated, single cells in the bone marrow. In contrast, p75 and TrkA were almost exclusively expressed by nerve fibers located nearby NGF+ blood vessels. The only non-neuronal expression of either p75 or TrkA in the femur was the expression of p75 by a subset of cells located in the deep and middle zone of the articular cartilage. Understanding the factors that tightly regulate the basal level of expression in normal bone and how the expression of NGF, TrkA, and p75 change in injury, disease, and aging may provide insights into novel therapies that can reduce skeletal pain and improve skeletal health.

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“…Moreover, it was assessed that dysregulated production of NGF determines proliferation of synovial cells influencing the inflammatory and proliferative cascades typical of inflammatory arthritis [110]. More recently, in accordance with Stoppiello et al who assessed increased synovial NGF in synovitis [115], Montagnoli et al confirmed a stage-related increase of β -NGF and its receptors in the inflammatory process of OA both in serum and synovial fluid [116].…”

Section: Ifp-synovial Membrane Mediators Involved In Oa Pathologymentioning

confidence: 95%

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

Belluzzi

Stocco

Pozzuoli

et al. 2019

BioMed Research International

129

124

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Osteoarthritis (OA) is the most common form of joint disease and a major cause of pain and disability in the adult population. Interestingly, there are patients with symptomatic OA displaying pain, while patients with asymptomatic OA that do not experience pain but show radiographic signs of joint damage. Pain is a complex experience integrating sensory, affective, and cognitive processes related to several peripheral and central nociceptive factors besides inflammation. During the last years, the role of infrapatellar fat pad (IFP), other than the synovial membrane, has been investigated as a potential source of pain in OA. Interestingly, new findings suggest that IFP and synovial membrane might act as a functional unit in OA pathogenesis and pain. The present review discuss the role of IFP and synovial membrane in the development of OA, with a particular focus on pain onset and the possible involved mediators that may play a role in OA pathology and pain mechanisms. Inflammation of IFP and synovial membrane may drive peripheral and central sensitization in KOA. Since sensitization is associated with pain severity in knee OA and may potentially contribute to the transition from acute to chronic, persistent pain in knee OA, preventing sensitization would be a potentially effective and novel means of preventing worsening of pain in knee OA.

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β-NGF and β-NGF receptor upregulation in blood and synovial fluid in osteoarthritis

Cited by 43 publications

References 40 publications

Changes in Nerve Growth Factor Expression and Macrophage Phenotype Following Intervertebral Disc Injury in Mice

Changes in Nerve Growth Factor Expression and Macrophage Phenotype Following Intervertebral Disc Injury in Mice

Immunohistochemical localization of nerve growth factor, tropomyosin receptor kinase A, and p75 in the bone and articular cartilage of the mouse femur

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

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