Matrix metalloproteinase (MMP)-8 is the most potent MMP for degrading collagen type-1 and plays an important role in inflammatory reactions and tissue remolding processes. MMP-8 is expressed mainly by polymorphonuclear leukocytes and is not expressed constitutively by most non-leukocytes. We studied the constitutive and TNF-α-induced expression of MMP-8 in cultured human uveal melanocytes (UM) and the relevant signal pathways involved. Conditioned media and cells were collected from UM and other cell types. MMP-8 proteins and mRNA were measured using ELISA kit, western blot and real time RT-PCR, respectively. Phosphorylated p38 MAPK, ERK1/2, and JNK1/2 were measured by ELISA kit and western blot. Very high levels of MMP-8 proteins and mRNA were detected in the conditioned media and cell lysates in 11 UM cell lines and three uveal melanoma cell lines cultured without serum, but not in media and cell lysates from other ocular resident cells or 12 malignant cell lines from other tissues, with exception of cutaneous melanoma cells. TNF-α moderately increased MMP-8 mRNA and protein levels in a dose- and time-dependent manner, accompanied by a significant increase of phosphorylated JNK1/2 and ERK1/2 in cell lysates. ERK1/2 (U0126) and JNK1/2 (SP600125) inhibitors significantly blocked TNF-α-induced and constitutive expression of MMP-8 in UM. This is the first report on the expression and secretion of MMP-8 by UM and uveal melanoma cells. The data suggest that UM may play a role in the remolding process and pathogenesis of inflammatory-related diseases in the eye via secretion of MMP-8.
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http://dx.doi.org/10.1016/j.exer.2018.06.023 | DOI Listing |
Alzheimers Dement
December 2024
Taipei Medical University, Taipei, Taiwan.
Understanding the physiological connection between platelets and brain function reveals new paradigms in neurodegenerative disease treatment. Platelets, traditionally associated with hemostasis, but also sometimes regarded as a mirror of neurons in the blood circulation, also encompass a spectrum of neurobiological roles, including neuroinflammation modulation, neurogenesis, and synaptic remodeling. These roles are primarily mediated through a rich array of bioactive molecules and extracellular vesicles (EVs), capable of traversing the blood-brain barrier.
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December 2024
University of Arizona, Tucson, AZ, USA.
Background: Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer's disease (AD) and may contribute to disease progression and severity. A pro-nitro-oxidative environment can lead to post-translational modifications of ion channels central to microvascular regulation in the brain, including the large conductance Ca-activated K channels (BK). Nitro-oxidative modulation of BK can resulting in decreased activity and vascular hyper-contractility, thus compromising neurovascular regulation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Georgia, Athens, GA, USA.
Background: Inflammatory cells play a key role in the pathophysiology of AD and other neurodegenerative disorders. Glycans are known to mediate inflammatory cell activation and migration yet very little is understood about the expression of glycans, glycoproteins, and other glycoconjugates at the CP which serves as a gateway for peripheral immune cells into the brain. In a familial AD mouse model, we observed increased expression of Siglec-F-recognized glycans on CP epithelial cells.
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December 2024
Department of Neurosurgery, Maxine Dunitz Neurosurgical Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Background: An emerging theory suggests a link between Alzheimer's disease (AD) and microbial infection. Notably, various microbes have been detected in the post-mortem brains of AD patients and murine models. However, there exists a gap in research concerning the presence and role of microbial infection in the AD retina, which shares common pathogenesis with the brain.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Center for Neurodegenerative Disease Research, PHILADELPHIA, PA, USA.
Background: Alzheimer's disease (AD) is pathologically defined by the presence of extracellular Aβ plaque and intracellular tau inclusions. Emerging evidence shows that tau aggregates contain pathogenic bioactivities of templating monomeric tau into filamentous fibrils and propagating through cells. Based on these findings, assays have been developed to detect minute amounts of pathogenic tau in human samples.
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