Astrocytic TLR4 expression and LPS-induced nuclear translocation of STAT3 in the sensory circumventricular organs of adult mouse brain

Nakano, Yousuke; Furube, Eriko; Morita, Shoko; Wanaka, Akio; Nakashima, Toshihiro; Miyata, Seiji

doi:10.1016/j.jneuroim.2014.12.013

Cited by 54 publications

(63 citation statements)

References 62 publications

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“…The following primary antibodies were used in the experiments: mouse monoclonal IgG against Math1 (Clone rabbit polyclonal IgG against Iba1 (dilution 1:700; WAKO Pure Chemical Industries, Osaka, Japan), oligodendrocyte transcription factor 2 (Olig2; dilution 1:500; Millipore, Billerica, MA, USA), Sox2 (dilution 1:2000; Millipore), S100β (dilution 1:3200; Yanaihara Institute, Shizuoka, J a p a n ) , V E G F -A ( d i l u t i o n 1 : 2 0 0 ; S a n t a C r u z Biotechnology), and VEGF-C (dilution 1:100; Abcam); guinea pig IgG against GFAP (YN-2011; dilution 1:400; Nakano et al 2015) and microtubule-associated protein 2 (MAP2, NH-2004;dilution;Taniguchi et al 2011). For nuclear staining, sections were incubated with 4′,6-diamidino-2-phenylindole (DAPI; 1 μg/ml; Dojindo, Kumamoto, Japan).…”

Section: Antibodies and Reagentsmentioning

confidence: 99%

“…Astrocytes cultured from S100ß-deficient mice exhibit enhanced Ca 2+ transients in response to treatment with KCl or caffeine, suggesting that S100ß plays a role in the maintenance of Ca 2+ homeostasis in astrocytes (Xiong et al 2000). In the sensory CVOs, Na + sensitive Na + channel Nax (Hiyama et al 2002), osmosensitive TRPV1 Ca 2+ channel (Mannari et al 2013), and LPS receptor TLR4 (Nakano et al 2015) have been Fig. 9 The effects of VEGF signaling inhibition on proliferation of OPCs.…”

Section: Profiles Of Nscs and Their Progenitor Cells In The Sensory Cvosmentioning

confidence: 99%

“…The peripheral administration of lipopolysaccharide (LPS) induces nuclear translocation of the signal transducer and activator of transcription factor 3 (STAT3) at astrocytes in the sensory CVOs (Harré et al 2002(Harré et al , 2003Gautron et al 2002;Rummel et al 2005). Recently, we have reported that TLR4 is specifically expressed at astrocytes, and that nuclear translocation of STAT3 is induced by central administration of LPS in the sensory CVOs (Nakano et al 2015).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of neural stem cells and their progeny in the sensory circumventricular organs of adult mouse

2015

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Although evidence has accumulated that neurogenesis and gliogenesis occur in the subventricular zone (SVZ) and subgranular zone (SGZ) of adult mammalian brains, recent studies indicate the presence of neural stem cells (NSCs) in adult brains, particularly the circumventricular regions. In the present study, we aimed to determine characterization of NSCs and their progenitor cells in the sensory circumventricular organs (CVOs), including organum vasculosum of the lamina terminalis, subfornical organ, and area postrema of adult mouse. There were two types of NSCs: tanycyte-like ependymal cells and astrocyte-like cells. Astrocyte-like NSCs proliferated slowly and oligodendrocyte progenitor cells (OPCs) and neural progenitor cells (NPCs) actively divided. Molecular marker protein expression of NSCs and their progenitor cells were similar to those reported in the SVZ and SGZ, except that astrocyte-like NSCs expressed S100β. These circumventricular NSCs possessed the capacity to give rise to oligodendrocytes and sparse numbers of neurons and astrocytes in the sensory CVOs and adjacent brain regions. The inhibition of vascular endothelial growth factor (VEGF) signaling by using a VEGF receptor-associated tyrosine kinase inhibitor AZD2171 largely suppressed basal proliferation of OPCs. A single systemic administration of lipopolysaccharide attenuated proliferation of OPCs and induced remarkable proliferation of microglia. The present study indicates that sensory circumventricular NSCs provide new neurons and glial cells in the sensory CVOs and adjacent brain regions.

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Section: Antibodies and Reagentsmentioning

confidence: 99%

Section: Profiles Of Nscs and Their Progenitor Cells In The Sensory Cvosmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterization of neural stem cells and their progeny in the sensory circumventricular organs of adult mouse

2015

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“…This does not, however, exclude the involvement of other mediators. In close proximity to the feeding regulatory centers in the brain are the circumventricular organs (CVOs), which may respond to inflammation since TLR4 is strongly up-regulated in the sensory CVOs in mice [197,198] and astrocyte-tanycytes in these regions have been shown to be responsive to LPS [46,197].…”

Section: Discussionmentioning

confidence: 99%

Mechanisms Behind Illness-Induced Anorexia

Nilsson¹

2016

Linköping University Medical Dissertations

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Loss of appetite is together with fever and malaise hallmarks of infection. Loosing appetite during an acute infection such as influenza does not result in any long-lasting effects, but loosing appetite during chronic diseases such as cancer or AIDS constitutes a risk factor for mortality. Food intake regulation during inflammation is orchestrated by the brain in response to peripheral inflammatory signals. It is known that expression of the prostaglandin synthesizing enzyme cyclooxygenase 2 (COX-2) is crucial for the mechanisms underlying inflammation-induced anorexia, and that prostaglandin E2 (PGE2) is involved in anorexia induced by interleukin-1 beta (IL-1β). In this thesis I examined the prostaglandin pathways proposed to be involved in anorexia. We show that acute anorexia is dependent on COX-2 expression, while cancer-induced anorexia is mediated by cyclooxygenase 1 (COX-1), at least in the initial stages, suggesting that the signaling pathways for chronic-and acute anorexia are distinct. We were able to demonstrate that the pathway underlying acute anorexia is distinct from that of fever, and that taste aversion is prostaglandin independent. We could also show that both acute and chronic anorexia-cachexia is dependent on expression of myeloid differentiation primary response gene (MyD88) in hematopoietic/myeloid cells. De generella slutsatser vi kan dra av studierna som ligger till grund för denna avhandling är att symptomen som vi upplever när vi blir sjuka, och som länge har ansetts ha samma bakomliggande signalvägar, till stor del signaleras till hjärnan på olika sätt. Aptitförlusten som uppkommer vid en infektion är inte alls lika beroende av ett specifikt prostaglandin, prostaglandin E2, som man tidigare trott, men en viktig faktor för att utveckla aptitförlust både vid akut-och kronisk sjukdom verkar vara MyD88-signallering i kroppens immunceller.Att kartlägga hur dessa signalvägar fungerar och vad som skiljer olika sjukdomssymptom åt är av stor vikt för utvecklingen av nya läkemedel. Dagens receptfria anti-inflammatoriska läkemedel är visserligen effektiva, men påverkar många av kroppens homeostatiska processer. Det är därför vanligt med allvarliga biverkningar såsom nedsatt hjärtfunktion och ökad risk för stroke och hjärtinfarkt, påverkan på njurfunktionen och magsår vid kronisk användning av dessa preparat. Önskvärt vore om det fanns läkemedel som endast påverkade de processer som missgynnar välmående.

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“…; Nakano et al . ). Interestingly, in spite of in vitro evidence showing that LPS directly activates sensory neurons (Ochoa‐Cortes et al .…”

Section: Introductionmentioning

confidence: 97%

Interaction between the hypothalamus and the immune system

Soto‐Tinoco

Guerrero‐Vargas

Buijs

2016

Experimental Physiology

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What is the topic of this review? Both branches of the autonomic nervous system are involved in the regulation of the inflammatory response. We explore how the hypothalamus may influence this process. What advances does it highlight? We analyse how a lipopolysaccharide signal is transmitted to the brain and which areas participate in the response of the brain to lipopolysaccharide. Recent studies show that the hypothalamus can influence the inflammatory response by modifying the autonomic output. The biological clock, the suprachiasmatic nucleus, is integrated into this circuit, putting a time stamp on the intensity of the inflammatory response. The brain is responsible for maintaining homeostasis of the organism, constantly adjusting its output via hormones and the autonomic nervous system to reach an optimal setting in every compartment of the body. Also, the immune system is under strong control of the brain. Apart from the conventional systemic responses evoked by the brain during inflammation, such as hypothalamic-pituitary-adrenal axis activation and the induction of sickness behaviour, the autonomic nervous system is now recognized to exert regulatory effects on the inflammatory response. Both branches of the autonomic nervous system are proposed to influence the inflammatory process. Here, we focus on those areas of the brain that might be involved in sensing inflammatory stimuli, followed by how that sensing could change the output of the autonomic nervous system in order to regulate the inflammatory response. Finally, we will discuss how the defenses of the body against a lipopolysaccharide challenge are organized by the hypothalamus.

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Astrocytic TLR4 expression and LPS-induced nuclear translocation of STAT3 in the sensory circumventricular organs of adult mouse brain

Cited by 54 publications

References 62 publications

Characterization of neural stem cells and their progeny in the sensory circumventricular organs of adult mouse

Characterization of neural stem cells and their progeny in the sensory circumventricular organs of adult mouse

Mechanisms Behind Illness-Induced Anorexia

Interaction between the hypothalamus and the immune system

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