| 1. |
Yamamoto S, Masuda T, Lipid in microglial biology - from material to mediator., Inflammation and Regeneration, 10.1186/s41232-023-00289-z, 2023.07. |
| 2. |
Masuda T, Recent topics regarding macrophage in the central nervous system, Journal of Biochemistry, 2022.11. |
| 3. |
Masuda T, Amann L, Prinz M, Novel insights into the origin and development of CNS macrophage subsets, Clin Transl Med, 2022.11. |
| 4. |
Paolicelli RC, Sierra A, Stevens B, Tremblay ME, Aguzzi A, Ajami B, Amit I, Audinat E, Bechmann I, Bennett M, Bennett F, Bessis A, Biber K, Bilbo S, Blurton-Jones M, Boddeke E, Brites D, Brône B, Brown GC, Butovsky O, Carson MJ, Castellano B, Colonna M, Cowley SA, Cunningham C, Davalos D, De Jager PL, de Strooper B, Denes A, Eggen BJL, Eyo U, Galea E, Garel S, Ginhoux F, Glass CK, Gokce O, Gomez-Nicola D, González B, Gordon S, Graeber MB, Greenhalgh AD, Gressens P, Greter M, Gutmann DH, Haass C, Heneka MT, Heppner FL, Hong S, Hume DA, Jung S, Kettenmann H, Kipnis J, Koyama R, Lemke G, Lynch M, Majewska A, Malcangio M, Malm T, Mancuso R, Masuda T, Matteoli M, McColl BW, Miron VE, Molofsky AV, Monje M, Mracsko E, Nadjar A, Neher JJ, Neniskyte U, Neumann H, Noda M, Peng B, Peri F, Perry VH, Popovich PG, Pridans C, Priller J, Prinz M, Ragozzino D, Ransohoff RM, Salter MW, Schaefer A, Schafer DP, Schwartz M, Simons M, Smith CJ, Streit WJ, Tay TL, Tsai LH, Verkhratsky A, von Bernhardi R, Wake H, Wittamer V, Wolf SA, Wu LJ, Wyss-Coray T, Microglia states and nomenclature: A field at its crossroads, Neuron, 10.1016/j.neuron.2022.10.020., 2022.11. |
| 5. |
Prinz M, Masuda T, Wheeler MA, Quintana FJ, Microglia and Central Nervous System-Associated Macrophages-From Origin to Disease Modulation, Annual Review of Immunology, 10.1146/annurev-immunol-093019-110159, 2021.04. |
| 6. |
Masuda T, Sankowski R, Staszewski O, Prinz M, Microglia Heterogeneity in the Single-Cell Era, Cell Reports, doi: 10.1016/j.celrep.2020.01.010., 30(5):1271-1281, 2020.02. |
| 7. |
Kierdorf K, Masuda T, Jordao M, Prinz M, Macrophages at CNS interfaces: ontogeny and function in health and disease, Nature Reviews Neuroscience, DOI: 10.1038/s41583-019-0201-x, 20(9):547-562, 2019.09. |
| 8. |
Masuda T, Prinz M, Microglia: A Unique Versatile Cell in the Central Nervous System, ACS Chemical Neuroscience, DOI: 10.1021/acschemneuro.5b00317, 7(4):428-34, 2016.04. |
| 9. |
Masuda T, Tsuda M, Inoue K, Transcriptional regulation in microglia and neuropathic pain, Pain Management, 6(2):91-4, 2016.04. |
| 10. |
Makoto Tsuda, Takahiro Masuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue, P2X4 receptors and neuropathic pain, Front Cell Neurosci., 2013.10, Neuropathic pain, a debilitating pain condition, is a common consequence of damage to the nervous system. Neuropathic pain is often resistant to currently available analgesics. A growing body of evidence indicates that spinal microglia react and undergo a series of changes that directly influence the establishment of neuropathic pain states. After nerve injury, P2X4 receptors (P2X4Rs) are upregulated in spinal microglia by several factors at the transcriptional and translational levels. Those include the CC chemokine CCL21 derived from damaged neurons, the extracellular matrix protein fibronectin in the spinal cord, and the transcription factor interferon regulatory factor 8 (IRF8) expressed in microglia. P2X4R expression in microglia is also regulated at the post-translational level by signaling from other cell-surface receptors such as CC chemokine receptor (CCR2). Importantly, inhibiting the function or expression of P2X4Rs and P2X4R-regulating molecules suppresses the aberrant excitability of dorsal horn neurons and neuropathic pain. These findings indicate that P2X4R-positive microglia are a central player in mechanisms for neuropathic pain. Thus, microglial P2X4Rs are a potential target for treating the chronic pain state.. |
| 11. |
Makoto Tsuda, Takahiro Masuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue, Microglial regulation of neuropathic pain, Journal of Pharmacological Sciences, 2013.01, Neuropathic pain is a highly debilitating chronic pain state that is a consequence of nerve injury or of diseases such as diabetes, cancer, infection, autoimmune disease, or trauma. Neuropathic pain is often resistant to currently available analgesics. There is a rapidly growing body of evidence indicating that signalings from spinal microglia play crucial roles in the pathogenesis of neuropathic pain. After peripheral nerve injury, microglia transform to reactive states through the expression of various genes such as cell-surface receptors (including purinergic receptors) and proinflammatory cytokines that enhance synaptic transmission in dorsal horn neurons. Inhibiting function or expression of these microglial molecules strongly suppresses pain hypersensitivity to innocuous mechanical stimuli (tactile allodynia), a hallmark symptom of neuropathic pain. A recent study also reveals that the transcription factor IRF8 (interferon regulatory factor 8) is a critical regulator of the nerve injury-induced gene expression in microglia. The present review article highlights the recent advances in our understanding of spinal microglia in neuropathic pain.. |
