Activin A stimulates mouse macrophages to express APRIL via the Smad3 and ERK/CREB pathways

Lee, Hwa-Joung; Seo, Goo-Young; Kim, Jaehee; Lee, Mi-Ra; Kim, Pyeung-Hyeun

doi:10.1016/j.imlet.2011.07.001

Cited by 12 publications

(7 citation statements)

References 37 publications

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“…ACTIVIN A treatment is thought to induce mesendoderm formation and the exit from pluripotency [ 8 , 43 ]. This expected result was confirmed with the changes in morphology, loss of TRA-1-60, increase in CXCR4 staining, and general induction of differentiation transcription patterns ( Fig 1A–1D ).…”

Section: Resultsmentioning

confidence: 99%

The Regulation of rRNA Gene Transcription during Directed Differentiation of Human Embryonic Stem Cells

et al. 2016

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It has become increasingly clear that proper cellular control of pluripotency and differentiation is related to the regulation of rRNA synthesis. To further our understanding of the role that the regulation of rRNA synthesis has in pluripotency we monitored rRNA synthesis during the directed differentiation of human embryonic stem cells (hESCs). We discovered that the rRNA synthesis rate is reduced ~50% within 6 hours of ACTIVIN A treatment. This precedes reductions in expression of specific stem cell markers and increases in expression of specific germ layer markers. The reduction in rRNA synthesis is concomitant with dissociation of the Pol I transcription factor, UBTF, from the rRNA gene promoter and precedes any increase to heterochromatin throughout the rRNA gene. To directly investigate the role of rRNA synthesis in pluripotency, hESCs were treated with the Pol I inhibitor, CX-5461. The direct reduction of rRNA synthesis by CX-5461 induces the expression of markers for all three germ layers, reduces the expression of pluripotency markers, and is overall similar to the ACTIVIN A induced changes. This work indicates that the dissociation of UBTF from the rRNA gene, and corresponding reduction in transcription, represent early regulatory events during the directed differentiation of pluripotent stem cells.

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Section: Resultsmentioning

confidence: 99%

The Regulation of rRNA Gene Transcription during Directed Differentiation of Human Embryonic Stem Cells

et al. 2016

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“…Similar activation of phosphorylation also occurs in CREB by phosphorylation at S133 (Lee et al . ). It has been shown that the phosphorylation of IKK, p65 S536, p65 S276, and CREB S133 can be mediated by ERK (Hu et al .…”

Section: Discussionmentioning

confidence: 97%

Endothelial Japanese encephalitis virus infection enhances migration and adhesion of leukocytes to brain microvascular endothelia via MEK‐dependent expression of ICAM1 and the CINC and RANTES chemokines

Lai

Chang

et al. 2012

Journal of Neurochemistry

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Currently, the underlying mechanisms and the specific cell types associated with Japanese encephalitis‐associated leukocyte trafficking are not understood. Brain microvascular endothelial cells represent a functional barrier and could play key roles in leukocyte central nervous system trafficking. We found that cultured brain microvascular endothelial cells were susceptible to Japanese encephalitis virus (JEV) infection with limited amplification. This type of JEV infection had negligible effects on cell viability and barrier integrity. Instead, JEV‐infected endothelial cells attracted more leukocytes adhesion onto surfaces and the supernatants promoted chemotaxis of leukocytes. Infection with JEV was found to elicit the elevated production of intercellular adhesion molecule‐1, cytokine‐induced neutrophil chemoattractant‐1, and regulated‐upon‐activation normal T‐cell expressed and secreted, contributing to the aforementioned leukocyte adhesion and chemotaxis. We further demonstrated that extracellular signal‐regulated kinase was a key upstream regulator which stimulated extensive endothelial gene induction by up‐regulating cytosolic phospholipase A2, NF‐κB, and cAMP response element‐binding protein via signals involving phosphorylation. These data suggest that JEV infection could activate brain microvascular endothelial cells and modify their characteristics without compromising the barrier integrity, making them favorable for the recruitment and adhesion of circulating leukocytes, thereby together with other unidentified barrier‐disrupting mechanisms contributing to Japanese encephalitis and associated neuroinflammation.

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“…The activin receptor is involved in activation of heterologous herpes simplex virus thymidine kinase [92] and plays a role in response to herpes type 8 [93]. Moreover activin A is involved in APRIL regulation and leads to stimulation of immune cells [94]. These two genes are downregulated in late infected spat and may be expressed at the beginning of the response to infection.…”

Section: Discussionmentioning

confidence: 99%

Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields

et al. 2013

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BackgroundMassive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality with OsHV-1 prevalence. Moreover, experimental infections using viral particles have documented the pathogenicity of OsHV-1 but the physiological responses of host to pathogen are not well known.ResultsThe aim of this study was to understand mechanisms brought into play against the virus during infection in the field. A microarray assay has been developed for a major part of the oyster genome and used for studying the host transcriptome across mortality on field. Spat with and without detectable OsHV-1 infection presenting or not mortality respectively were compared by microarray during mortality episodes. In this study, a number of genes are regulated in the response to pathogen infection on field and seems to argue to an implication of the virus in the observed mortality. The result allowed establishment of a hypothetic scheme of the host cell’s infection by, and response to, the pathogen.ConclusionsThis response shows a “sensu stricto” innate immunity through genic regulation of the virus OsHV-1 life cycle, but also others biological processes resulting to complex interactions between host and pathogens in general.

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Activin A stimulates mouse macrophages to express APRIL via the Smad3 and ERK/CREB pathways

Cited by 12 publications

References 37 publications

The Regulation of rRNA Gene Transcription during Directed Differentiation of Human Embryonic Stem Cells

The Regulation of rRNA Gene Transcription during Directed Differentiation of Human Embryonic Stem Cells

Endothelial Japanese encephalitis virus infection enhances migration and adhesion of leukocytes to brain microvascular endothelia via MEK‐dependent expression of ICAM1 and the CINC and RANTES chemokines

Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields

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