Literature DB >> 15148607

Cellular expression of murine Ym1 and Ym2, chitinase family proteins, as revealed by in situ hybridization and immunohistochemistry.

Junko Nio1, Wakako Fujimoto, Akihiro Konno, Yasuhiro Kon, Makoto Owhashi, Toshihiko Iwanaga.   

Abstract

Ym is one of the chitinase family proteins, which are widely distributed in mammalian bodies and can bind glycosaminoglycans such as heparin/heparan sulfate. Ym1 is a macrophage protein produced in parasitic infections, while its isoform, Ym2, is upregulated in lung under allergic conditions. In the present study, we revealed the distinct cellular expression of Ym1 and Ym2 in normal mice by in situ hybridization and immunohistochemistry. Ym1 was principally expressed in the lung, spleen, and bone marrow, while Ym2 was found in the stomach. Ym1-expressing cells in the lung were alveolar macrophages, and the immunoreactivity for Ym1 was localized in rough endoplasmic reticulum. In the spleen, Ym1-expressing cells gathered in the red pulp and were electron microscopically identified as immature neutrophils. In the bone marrow, immature neutrophils were intensely immunoreactive, but lost this immunoreactivity with maturation. Moreover, needle-shaped crystals in the cytoplasm of macrophages, which formed erythroblastic islands, also showed intense Ym1 immunoreactivity. Ym2 expression was restricted to the stratified squamous epithelium in the junctional region between forestomach and glandular stomach. The function of Ym1 and Ym2 is still unclear; however, the distinct cellular localization under normal conditions suggests their important roles in hematopoiesis, tissue remodeling, or immune responses as an endogenous lectin.

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Year:  2004        PMID: 15148607     DOI: 10.1007/s00418-004-0654-4

Source DB:  PubMed          Journal:  Histochem Cell Biol        ISSN: 0948-6143            Impact factor:   4.304


  27 in total

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  23 in total

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9.  The pathogenesis of chronic eosinophilic esophagitis in SHARPIN-deficient mice.

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10.  Development of chronic bronchitis and emphysema in beta-epithelial Na+ channel-overexpressing mice.

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