Epidermal Growth Factor Receptor Expression in Skin Does Not Predict Dementia in the Elderly

Styren, Scot; Styren, Gisele C.; DeKosky, Steven T.

doi:10.1159/000017016

Cited by 6 publications

(3 citation statements)

References 16 publications

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“…Aberrant expression of TGM2 [640], NEUROD1 [641], PRKG2 [642], RIT2 [324], TLR2 [643], MYRF (myelin regulatory factor) [642], SIRT2 [644], MMP3 [645], CASP1 [646], POU3F2 [647] and COMT (catechol-O-methyltransferase) [648] have been observed in HD. SERPINA1 [521], LRRK2 [649], TF (transferrin) [650], REN (renin) [651], TLR2 [652], MOBP (myelin associated oligodendrocyte basic protein) [653], SYK (spleen associated tyrosine kinase) [654], MBP (myelin basic protein) [625], SHH (sonic hedgehog signaling molecule) [655], RBP4 [590], SNCB (synuclein beta) [543], MMP3 [656], VWF (von Willebrand factor) [657], EGFR (epidermal growth factor receptor) [658], ABCA1 [659] and GPR39 [618] are associated with the clinical stages of dementia. Altered expression of LRRK2 [660], GPR17 [661], TF (transferrin) [662], NEUROD1 [663], RELN (reelin) [664], LCP1 [665], TFAP2B [666], HOXA5 [667], MSR1 [668], REN (renin) [669], OLIG2 [670], TLR2 [671], WT1 [672], SLC22A3 [673], CADM2 [674], PRKCH (protein kinase C eta) [675], MBP (myelin basic protein) [676], XAF1 [677], GPR37 [678], SHH (sonic hedgehog signaling molecule) [679], VTN (vitronectin) [680], SIRT2 [681], RBP4 [682], BMP2 [683], CDH13 [684], NR3C2 [685], TRPC6 [686], MMP3 [687], FGF19 [688], HLA-DRB1 [689], CD74 [690], VWF (von Willebrand factor) [691], ANGPT2 [692], CHRDL1 [693], AKR1C3 [694], NEDD4L [695], CASP1 [696], PDE2A [697], GAS7 [698], TET1 [699], EFNB2 [700], EGFR (epidermal growth factor receptor) [701<...…”

Section: Discussionmentioning

confidence: 99%

“…LRRK2 [620], EGFR (epidermal growth factor receptor) [636] and NEDD4L [632] are critical in amyotrophic lateral sclerosis development. In many clinical studies, LRRK2 [649] and EGFR (epidermal growth factor receptor) [658] have been linked to the start of dementia. LRRK2 [660], EGFR (epidermal growth factor receptor) [701], NEDD4L [695], COMT (catechol-O-methyltransferase) [705] and CDK18 [737] are involved in the regulation of stroke.…”

Section: Discussionmentioning

confidence: 99%

“…MAP1B [637], EGFR (epidermal growth factor receptor) [636], NEDD4L [632], hsa-mir-21-5p [771], ATF3 [772] and SREBF1 [773] were significantly altered in patients with amyotrophic lateral sclerosis. A previous study reported that the EGFR (epidermal growth factor receptor) [658], hsa-mir-21-5p [762] and SREBF1 [774] biomarkers were associated with the dementia. Previous studies have shown that EGFR (epidermal growth factor receptor) [701], NEDD4L [695], hsa-mir-21-5p [775] and ATF3 [776] are closely associated with stroke.…”

Section: Discussionmentioning

confidence: 99%

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Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms of HD pathogenesis are largely unknown. This investigation aims to identify the hub genes, miRNA and TFs in HD and explore their potential molecular regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), Gene ontology and REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network and module analysis, miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network analysis, and receiver operating characteristic curve (ROC) analysis were applied to identify hub genes, miRNA and TFs, and key drivers of HD pathogenesis. We identified 958 DEGs in the discovery phase, consisting of 479 up regulated genes and 479 down regulated genes. GO and REACTOME enrichment analyses of the 479 up regulated genes and 479 down regulated genes showed that they were mainly involved in multicellular organismal process, developmental process, signaling by GPCR and MHC class II antigen presentation. Further analysis of the PPI network using Cytoscape and PEWCC plugins identified 10 hub genes, including LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L and COMT. Possible target miRNAs and TFs, including hsa-mir-1292-5p, hsa-mir-4521, ESRRB and SREBF1, were predicted by constructing a miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network. This investigation used bioinformatics methods to explore the molecular pathogenesis of HD, and identified potential molecular markers. These molecular markers might provide novel ideas and methods for the early diagnosis, treatment, and monitoring of HD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Selective adenosine A2a receptor antagonism reduces JNK activation in oligodendrocytes after cerebral ischaemia

Melani

Cipriani

Vannucchi

et al. 2009

Brain

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Adenosine is a potent biological mediator, the concentration of which increases dramatically following brain ischaemia. During ischaemia, adenosine is in a concentration range (muM) that stimulates all four adenosine receptor subtypes (A(1), A(2A), A(2B) and A(3)). In recent years, evidence has indicated that the A(2A) receptor subtype is of critical importance in stroke. We have previously shown that 24 h after medial cerebral artery occlusion (MCAo), A(2A) receptors up-regulate on neurons and microglia of ischaemic striatum and cortex and that subchronically administered adenosine A(2A) receptor antagonists protect against brain damage and neurological deficit and reduce activation of p38 mitogen-activated protein kinase (MAPK) in microglial cells. The mechanisms by which A(2A) receptors are noxious during ischaemia still remain elusive. The objective of the present study was to investigate whether the adenosine A(2A) antagonist SCH58261 affects JNK and MEK1/ERK MAPK activation. A further aim was to investigate cell types expressing activated JNK and MEK1/ERK MAPK after ischaemia. We hereby report that the selective adenosine A(2A) receptor antagonist, SCH58261, administered subchronically (0.01 mg/kg i.p) 5 min, 6 and 20 h after MCAo in male Wistar rats, reduced JNK MAPK activation (immunoblot analysis: phospho-JNK54 isoform by 81% and phospho-JNK46 isoform by 60%) in the ischaemic striatum. Twenty-four hours after MCAo, the Olig2 transcription factor of oligodendroglial progenitor cells and mature oligodendrocytes was highly expressed in cell bodies in the ischaemic striatum. Immunofluorescence staining showed that JNK MAPK is maximally expressed in Olig2-stained oligodendrocytes and in a few NeuN stained neurons. Striatal cell fractioning into nuclear and extra-nuclear fractions demonstrated the presence of Olig2 transcription factor and JNK MAPK in both fractions. The A(2A) antagonist reduced striatal Olig 2 transcription factor (immunoblot analysis: by 55%) and prevented myelin disorganization, assessed by myelin-associated glycoprotein staining. Twenty-four hours after MCAo, ERK1/2 MAPK was highly activated in the ischaemic striatum, mostly in microglia, while it was reduced in the ischaemic cortex. The A(2A) antagonist did not affect activation of the ERK1/2 pathway. The efficacy of A(2A) receptor antagonism in reducing activation of JNK MAPK in oligodendrocytes suggests a mechanism of protection consisting of scarring oligodendrocyte inhibitory molecules that can hinder myelin reconstitution and neuron functionality.

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Brief screening tests during acute admission in patients with mild stroke are predictive of vascular cognitive impairment 3–6 months after stroke

Dong

Venketasubramanian

Chan

et al. 2012

J Neurol Neurosurg Psychiatry

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Epidermal Growth Factor Receptor Expression in Skin Does Not Predict Dementia in the Elderly

Cited by 6 publications

References 16 publications

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Selective adenosine A2a receptor antagonism reduces JNK activation in oligodendrocytes after cerebral ischaemia

Brief screening tests during acute admission in patients with mild stroke are predictive of vascular cognitive impairment 3–6 months after stroke

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