It is known that total endothelial nitric oxide synthase (eNOS) is localized in peripheral nerve fibers, but the existence of the phosphorylation site/s of eNOS in peripheral nerve fibers is unknown. In the perfusion-fixed and decalcified sections of rat palates, eNOS and eNOS phosphorylated at Ser(116) were identified in the nerve fibers of the glandulae palatinae. The localization of eNOS phosphorylated at Ser(1177) and Thr(495) in nerve fibers was undetectable. It is concluded that eNOS is phosphorylated at Ser(116) in nerve fibers of the glandulae palatinae under basal conditions. The basal Ser(1177) and Thr(495) phosphorylation of eNOS are missing in nerve fibers of the glandulae palatinae.
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http://dx.doi.org/10.1016/j.neulet.2004.03.045 | DOI Listing |
J Cell Mol Med
February 2025
Department of Neurobiology, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, China.
Myelin is the key structure for high-speed information transmission and is formed by oligodendrocytes (OLs) which are differentiated from oligodendrocyte precursor cells (OPCs) in the central nervous system. Lipid is the main component of myelin and the role of lipid metabolism-related molecules in myelination attach increasing attention. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) mediates the conversion of lysophosphatidylcholine (LPC) to phosphatidylcholine (PC), and its role in myelination draws our interest as LPC is a classical demyelination inducer and PC is a major component of myelin.
View Article and Find Full Text PDFFront Immunol
January 2025
Neuroimmunology Research Group, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.
Introduction: Remyelination of demyelinated axons can occur as an endogenous repair mechanism in multiple sclerosis (MS), but its efficacy varies between both MS individuals and lesions. The molecular and cellular mechanisms that drive remyelination remain poorly understood. Here, we studied the relation between microglia activation and remyelination activity in MS.
View Article and Find Full Text PDFMuscle Nerve
January 2025
Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Introduction: Mixed connective tissue disease (MCTD) patients often have myositis, however, myopathological and clinical data for MCTD are limited. Recent reports have shown that the pathology of MCTD myositis resembles that of immune-mediated necrotizing myopathy (IMNM), whereas earlier reports described perifascicular atrophy or inflammatory infiltrates predominantly in the perivascular region in MCTD myositis. We aim to describe the clinical and myopathological features of MCTD myositis.
View Article and Find Full Text PDFBrain
January 2025
Department of Neurology, National Taiwan University Hospital, Taipei, 100225, Taiwan.
Hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) is a neurodegenerative disease caused by mutations in the gene encoding transthyretin (TTR). Despite amyloid deposition being pathognomonic for diagnosis, this pathology in nervous tissues cannot fully account for nerve degeneration, implying additional pathophysiology for neurodegeneration, which, however, has not yet been fully elucidated. In this study, neuroinflammation in ATTRv-PN was investigated by examining nerve morphometry, the blood-nerve barrier, and macrophage infiltration in the sural nerves of ATTRv-PN patients and the sciatic nerves of a complementary mouse system, i.
View Article and Find Full Text PDFBurns Trauma
January 2025
Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, Lishui, Zhejiang 323000, China.
Neuroregulation during skin wound healing involves complex interactions between the nervous system and intricate tissue repair processes. The skin, the largest organ, depends on a complex system of nerves to manage responses to injury. Recent research has emphasized the crucial role of neuroregulation in maximizing wound healing outcomes.
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