2019
DOI: 10.1111/bpa.12798
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Complement C3a induces axonal hypomyelination in the periventricular white matter through activation of WNT/β‐catenin signal pathway in septic neonatal rats experimentally induced by lipopolysaccharide

Abstract: Neuroinflammation is thought to play a pivotal role in the pathogenesis of periventricular white matter (PWM) damage (PWMD) induced by neonatal sepsis. Because the complement cascade is implicated in inflammatory response, this study was carried out to determine whether C3a is involved in PWMD, and, if so, whether it would induce axonal hypomyelination. Furthermore, we explored if C3a would act through its C3a receptor (C3aR) and thence inhibit maturation of oligodendrocyte precursor cells (OPCs) via the WNT/β… Show more

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Cited by 29 publications
(39 citation statements)
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“…Previous studies in cultured cancer cell lines suggest that DDX5 promotes oncogene expressions downstream of β-catenin [41,42]. Here, our in vivo studies revealed an unappreciated role of DDX5 in promoting the expression of complement protein C3, a potent inducer of the Wnt/β-catenin cascade that drives tumorigenesis in the colon [44].…”
Section: Discussionsupporting
confidence: 53%
“…Previous studies in cultured cancer cell lines suggest that DDX5 promotes oncogene expressions downstream of β-catenin [41,42]. Here, our in vivo studies revealed an unappreciated role of DDX5 in promoting the expression of complement protein C3, a potent inducer of the Wnt/β-catenin cascade that drives tumorigenesis in the colon [44].…”
Section: Discussionsupporting
confidence: 53%
“…Our study revealed that the knockdown of CLDN-1 or CLDN-3 could inhibit myelinogenesis. The expression levels of myelin proteins such as PLP and MBP are significantly reduced in the white matter, and the number of PLP-positive and MBPpositive cells markedly decrease, which result in the reduction of myelin sheath thickness, and subsequently, LA (45,46). The molecular mechanism underlying the basic promoter activity of PLP and MBP depend on AKT activation (47,48), and CLDN-1 or CLDN-3 knockdown can significantly inhibit AKT activity (41,49).…”
Section: ' Discussionmentioning
confidence: 99%
“…Therefore, the reduction of the expression levels of CLDN-1 and CLDN-3 in LA patients may attenuate MBP and PLP synthesis by downregulating AKT signaling. Besides, the increased levels of phosphorylated-AKT promotes Wnt/b-catenin/Tcf4 signal transduction; this inhibits OLIG2, SOX10, PLP, and MBP expression in OPCs (46). The differentiation or maturation of OPCs is regulated by the transcription factors OLIG1, OLIG2, NKX2.2, and SOX10 (50).…”
Section: ' Discussionmentioning
confidence: 99%
“…NG2 is a type-1 membrane protein, which is expressed by OPCs [25]. OPCs gradually differentiated into mature oligodendrocytes labeled CNPase or PLP under the action of differentiation promoting transcription factors [26,27]. The maturation of OPCs plays an important role in the myelination of targeting axons.…”
Section: Discussionmentioning
confidence: 99%