Neuroinflammatory and Amyloidogenic Activities of IL-32β in Alzheimer’s Disease

Yun, Hyung-Mun; Kim, Jin A.; Hwang, Chul Ju; Jin, Peng; Baek, Myung Ki; J, Lee; Hong, Juhee; Lee, Sang Min; Han, Sang Bae; Oh, Ki Wan; Choi, Dong Young; Yoon, Do Young; Hong, Jin Tae

doi:10.1007/s12035-014-8860-0

Cited by 19 publications

(15 citation statements)

References 46 publications

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“…The activation of gp130 causes phosphorylation and activation of JAK2/STAT3 cascade and the subsequent increase in GFAP expression (Yanagisawa, Nakashima, & Taga, 1999). This signaling cascade in astrocytes has been identified in studies of cardiotrophin-1 signaling in development (Ochiai, Yanagisawa, Takizawa, Nakashima, & Taga, 2001), neuropoietin action in neuroepithelial cells (Ohno et al, 2006), cerebral ischemia and spinal cord injury (Oliva et al, 2012), neuroinflammation and amyloidogenesis (Yun et al, 2015), and intracerebral hemorrhage . Thus, gp130-JAK2/STAT3 cascade is a highly representative regulatory pathway for neurochemical regulation of GFAP expression.…”

Section: Jak2/stat3 Cascadementioning

confidence: 94%

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Liu

et al. 2019

Glia

115

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Glial fibrillary acidic protein (GFAP), a type III intermediate filament, is a marker of mature astrocytes. The expression of GFAP gene is regulated by many transcription factors (TFs), mainly Janus kinase‐2/signal transducer and activator of transcription 3 cascade and nuclear factor κ‐light‐chain‐enhancer of activated B cell signaling. GFAP expression is also modulated by protein kinase and other signaling molecules that are elicited by neuronal activity and hormones. Abnormal expression of GFAP proteins occurs in neuroinflammation, neurodegeneration, brain edema‐eliciting diseases, traumatic brain injury, psychiatric disorders and others. GFAP, mainly in α‐isoform, is the major component of cytoskeleton and the scaffold of astrocytes, which is essential for the maintenance of astrocytic structure and shape. GFAP also has highly morphological plasticity because of its quick changes in assembling and polymerizing states in response to environmental challenges. This plasticity and its corresponding cellular morphological changes endow astrocytes the functions of physical barrier between adjacent neurons and stabilizer of extracellular environment. Moreover, GFAP colocalizes and even molecularly associates with many functional molecules. This feature allows GFAP to function as a platform for direct interactions between different molecules. Last, GFAP involves transportation and localization of other functional proteins and thus serves as a protein transport guide in astrocytes. This guiding role of GFAP involves an elastic retraction and extension cytoskeletal network that couples with GFAP reassembling, transporting, and membrane protein recycling machinery. This paper reviews our current understanding of the expression and functions of GFAP as well as their regulation.

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Section: Jak2/stat3 Cascadementioning

confidence: 94%

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Liu

et al. 2019

Glia

115

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“…Oligomeric Aβ has also been revealed to encourage the formation of ROS in primary cortical and hippocampal neurons [ 125 ], which has been connected with inflammation and neurodegeneration. Aβ may perhaps indirectly induce neurotoxicity via the stimulation of proinflammatory responses [ 126 ], caspase-8 [ 127 ] and ROS [ 128 ] which might have a role in restraining the formation of hippocampal memory [ 129 ]. Nonetheless, the majority of the direct effect of Aβ in on synaptic degeneration through its action on precise signaling cascades.…”

Section: Toxin-induced Experimental Models Of Memory Impairmentmentioning

confidence: 99%

Toxin-Induced Experimental Models of Learning and Memory Impairment

Kumar

Cho

et al. 2016

IJMS

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Animal models for learning and memory have significantly contributed to novel strategies for drug development and hence are an imperative part in the assessment of therapeutics. Learning and memory involve different stages including acquisition, consolidation, and retrieval and each stage can be characterized using specific toxin. Recent studies have postulated the molecular basis of these processes and have also demonstrated many signaling molecules that are involved in several stages of memory. Most insights into learning and memory impairment and to develop a novel compound stems from the investigations performed in experimental models, especially those produced by neurotoxins models. Several toxins have been utilized based on their mechanism of action for learning and memory impairment such as scopolamine, streptozotocin, quinolinic acid, and domoic acid. Further, some toxins like 6-hydroxy dopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and amyloid-β are known to cause specific learning and memory impairment which imitate the disease pathology of Parkinson’s disease dementia and Alzheimer’s disease dementia. Apart from these toxins, several other toxins come under a miscellaneous category like an environmental pollutant, snake venoms, botulinum, and lipopolysaccharide. This review will focus on the various classes of neurotoxin models for learning and memory impairment with their specific mechanism of action that could assist the process of drug discovery and development for dementia and cognitive disorders.

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“…For 4′,6′-diamidino-2phenylindole dihydrochloride (DAPI) staining, the slides were incubated for 15 min at room temperature in the dark with a mounting medium for fluorescence containing DAPI (Vector Laboratories). The tissues were then examined via fluorescence microscopy (Leica Microsystems AG, Wetzlar, Germany), and the nuclei were visualized via DAPI staining [56].…”

Section: Tunel Assaymentioning

confidence: 99%

Prevention of multiple system atrophy using human bone marrow-derived mesenchymal stem cells by reducing polyamine and cholesterol-induced neural damages

et al. 2020

Self Cite

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Background: Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder of unknown etiology, but is closely associated with damage to dopaminergic neurons. MSA progression is rapid. Hence, long-term drug treatments do not have any therapeutic benefits. We assessed the inhibitory effect of mesenchymal stem cells (MSCs) on double-toxin-induced dopaminergic neurodegenerative MSA. Results: Behavioral disorder was significantly improved and neurodegeneration was prevented following MSC transplantation. Proteomics revealed lower expression of polyamine modulating factor-binding protein 1 (PMFBP1) and higher expression of 3-hydroxymethyl-3-methylglutaryl-CoA lyase (HMGCL), but these changes were reversed after MSC transplantation. In the in vitro study, the 6-OHDA-induced effects were reversed following co-culture with MSC. However, PMFBP1 knockdown inhibited the recovery effect due to the MSCs. Furthermore, HMGCL expression was decreased following co-culture with MSCs, but treatment with recombinant HMGCL protein inhibited the recovery effects due to MSCs. Conclusions: These data indicate that MSCs protected against neuronal loss in MSA by reducing polyamine-and cholesterol-induced neural damage.

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Neuroinflammatory and Amyloidogenic Activities of IL-32β in Alzheimer’s Disease

Cited by 19 publications

References 46 publications

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Toxin-Induced Experimental Models of Learning and Memory Impairment

Prevention of multiple system atrophy using human bone marrow-derived mesenchymal stem cells by reducing polyamine and cholesterol-induced neural damages

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