Accumulation of Ym1/2 protein in the mouse olfactory epithelium during regeneration and aging

Giannetti, Nathalie; Moyse, Emmanuel; Ducray, Angélique; Bondier, Jean‐Robert; Jourdan, F; Propper, Alain; Kästner, Anne

doi:10.1016/j.neuroscience.2003.09.024

Cited by 35 publications

(26 citation statements)

References 62 publications

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“…Next to Arg1, Ym1 is another established marker for microglia alternative activation [2,44]. Ym1 is a heparin/heparin sulphate-binding lectin that is transiently expressed during inflammation [44] and although the precise functions of Ym1 remain elusive, recent reports have suggested an involvement in tissue remodelling and regulation of inflammation [45,46]. …”

Section: Discussionmentioning

confidence: 99%

TGFβ signalling plays an important role in IL4-induced alternative activation of microglia

Zhou

Spittau

Krieglstein

2012

J Neuroinflammation

141

114

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BackgroundMicroglia are the resident immune cells of the central nervous system and are accepted to be involved in a variety of neurodegenerative diseases. Several studies have demonstrated that microglia, like peripheral macrophages, exhibit two entirely different functional activation states, referred to as classical (M1) and alternative (M2) activation. TGFβ is one of the most important anti-inflammatory cytokines and its effect on inhibiting microglia or macrophage classical activation has been extensively studied. However, the role of TGFβ during alternative activation of microglia has not been described yet.MethodsTo investigate the role of TGFβ in IL4-induced microglia alternative activation, both, BV2 as well as primary microglia from new born C57BL/6 mice were used. Quantitative RT-PCR and western blots were performed to detect mRNA and protein levels of the alternative activation markers Arginase1 (Arg1) and Chitinase 3-like 3 (Ym1) after treatment with IL4, TGFβ or both. Endogenous TGFβ release after IL4 treatment was evaluated using the mink lung epithelial cell (MLEC) assay and a direct TGFβ2 ELISA. TGFβ receptor type I inhibitor and MAPK inhibitor were applied to address the involvement of TGFβ signalling and MAPK signalling in IL4-induced alternative activation of microglia.ResultsTGFβ enhances IL4-induced microglia alternative activation by strongly increasing the expression of Arg1 and Ym1. This synergistic effect on Arg1 induction is almost completely blocked by the application of the MAPK inhibitor, PD98059. Further, treatment of primary microglia with IL4 increased the expression and secretion of TGFβ2, suggesting an involvement of endogenous TGFβ in IL4-mediated microglia activation process. Moreover, IL4-mediated induction of Arg1 and Ym1 is impaired after blocking the TGFβ receptor I indicating that IL4-induced microglia alternative activation is dependent on active TGFβ signalling. Interestingly, treatment of primary microglia with TGFβ alone results in up regulation of the IL4 receptor alpha, indicating that TGFβ increases the sensitivity of microglia for IL4 signals.ConclusionsTaken together, our data reveal a new role for TGFβ during IL4-induced alternative activation of microglia and consolidate the essential functions of TGFβ as an anti-inflammatory molecule and immunoregulatory factor for microglia.

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Section: Discussionmentioning

confidence: 99%

TGFβ signalling plays an important role in IL4-induced alternative activation of microglia

Zhou

Spittau

Krieglstein

2012

J Neuroinflammation

141

114

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“…It was then demonstrated that salt solutions as Zn sulfate induce an extensive degeneration of the olfactory epithelium (Cancalon, 1982) including a significant loss of olfactory neurons followed by a substantial regeneration (Burd, 1993;Ducray et al, 2002;Giannetti et al, 2004;Herzog et al, 1999). This molecule has been used in our laboratory to study both the kinetics of epithelium regeneration as a function of the time spent after a single instillation in the nostril and after that the recovery of odor discrimination in mice (Ducray et al, 2002).…”

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confidence: 99%

Harmful Effects of Cadmium on Olfactory System in Mice

Bondier

Michel

Propper

et al. 2008

Inhalation Toxicology

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The inhalation of certain metals can result in olfactory epithelial injury, an altered sense of smell, and direct delivery of the metal from the olfactory epithelium to the olfactory bulbs and other parts of the central nervous system. The purpose of this study was to examine whether mice given an intranasal instillation of cadmium would develop altered olfactory function and to assess whether cadmium may be transported directly from the olfactory epithelium to the central nervous system. To evaluate cadmium's ability to induce anosmia and on the basis of olfactory epithelium sensitivity to metals, the aim of this study was first to study cadmium effects on the olfactory function and secondly to check whether cadmium may be transported from the nasal area to the central nervous system. After an intranasal instillation of a solution containing CdCl 2 at 136 mM, we observed in treated mice: (1) a partial destruction of the olfactory epithelium, which is reduced to three or four basal cell layers followed by a progressive regeneration; (2) a loss of odor discrimination with a subsequent recovery; and (3) a cadmium uptake by olfactory bulbs demonstrated using atomic absorption spectrophotometry, but not by other parts of the central nervous system. Cadmium was delivered to the olfactory bulbs, most likely along the olfactory nerve, thereby bypassing the intact blood-brain barrier. We consider that cadmium can penetrate olfactory epithelium and hence be transported to olfactory bulbs. The olfactory route could therefore be a likely way to reach the brain and should be taken into account for occupational risk assessments for this metal.

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“…CLP genes have been reported from human, goat, rat, and D. melanogaster individuals (Bleau et al, 1999;Kawamura et al, 1999;Giannetti et al, 2004;Kelleher et al, 2005;Recklies et al, 2005;Johansen, 2006;Arakane and Muthukrishnan, 2010). However, research on the characterization of CLPs has been limited in the Japanese scallop and mollusks, in general.…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, YKL-40 [a CLP also referred to as a chitinase 3-like-1 and human cartilage glycoprotein-39 (HC-gp39)] was first identified in mouse breast cancer cells and named BRP-39 (Bleau et al, 1999). YKL-40, which has been significantly correlated with the severity of asthma, plays an important role in the homeostasis of several organs in humans, where it regulates tissue remodeling as well as cell proliferation and survival in response to pathological conditions (Giannetti et al, 2004;Kelleher et al, 2005;Recklies et al, 2005;Johansen, 2006). In mollusks, 3 CLPs (Cg-Clp1, Cg-Clp2, and Cg-Clp3) have been identified from the oyster Crassostrea gigas (Badariotti et al, 2006(Badariotti et al, , 2007(Badariotti et al, , 2011.…”

Section: Introductionmentioning

confidence: 99%

Identification and expression analysis of cDNA encoding chitinase-like protein (CLP) gene in Japanese scallop Mizuhopecten yessoensis

Gao¹,

Xu²,

Su³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Chitinase-like proteins (CLP) are important members of the glycoside hydrolase family 18 (GH18) and are involved in growth control and remodeling processes. In this study, a CLP transcript was isolated and sequenced from the Japanese scallop (Mizuhopecten yessoensis) after screening expressed sequence tags. The full-length complementary DNA of M. yessoensis CLP (My-Clp1) was 1555 bp in length, consisting of a 75-bp 5'-untranslated region (UTR), a 160-bp 3'-UTR, and a 1320-bp open reading frame bearing characteristics of the GH18 family. The My-Clp1 protein was well conserved, with similar domain structures and architecture across species (e.g., from mollusks to mammals). Expression analysis in healthy tissues and across developmental stages revealed a strong preference for expression; My-Clp1 was abundantly expressed in the mantle and throughout metamorphosis, which suggests the involvement of My-Clp1 in the synthesis of extracellular components, and tissue degeneration and remodeling. My-Clp1 expression was induced after infection with a bacterial pathogen, Vibrio anguillarum, suggesting its involvement in immunity against this intracellular pathogen.

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Accumulation of Ym1/2 protein in the mouse olfactory epithelium during regeneration and aging

Cited by 35 publications

References 62 publications

TGFβ signalling plays an important role in IL4-induced alternative activation of microglia

TGFβ signalling plays an important role in IL4-induced alternative activation of microglia

Harmful Effects of Cadmium on Olfactory System in Mice

Identification and expression analysis of cDNA encoding chitinase-like protein (CLP) gene in Japanese scallop Mizuhopecten yessoensis

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