Expression and immunohistochemical localization of galectin‐3 in various mouse tissues

Kim, Heechul; Lee, Won Jin; Hyun, Jin Won; Park, Jae-Woo; Joo, Hong‐Gu; Shin, Taekyun

doi:10.1016/j.cellbi.2006.11.036

Cited by 100 publications

(73 citation statements)

References 15 publications

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“…15 It has been proposed that Gal-3 interacts with numerous ligands such as cell surface receptors (integrins) and ECM proteins (collagen, elastin, fibronectin). 16 The expression of Gal-3 has been reported in many tissues 17 (including myocardium). Gal-3 is expressed in fibroblasts, 18 endothelial cells, 19,20 and inflammatory cells such as macrophages 21 which appear to be involved in most models of injury.…”

mentioning

confidence: 99%

Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

Calvier

Miana

Reboul

et al. 2013

ATVB

326

278

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Objective-Aldosterone (Aldo) is involved in arterial stiffness and heart failure, but the mechanisms have remained unclear. Galectin-3 (Gal-3), a β-galactoside-binding lectin, plays an important role in inflammation, fibrosis, and heart failure. We investigated here whether Gal-3 is involved in Aldo-induced vascular fibrosis. Methods and Results-In rat vascular smooth muscle cells Gal-3 overexpression enhanced specifically collagen type I synthesis. Moreover Gal-3 inhibition by modified citrus pectin or small interfering RNA blocked Aldo-induced collagen type I synthesis. Rats were treated with Aldo-salt combined with spironolactone or modified citrus pectin for 3 weeks. Hypertensive Aldo-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Spironolactone or modified citrus pectin treatment reversed all the above effects. Wild-type and Gal-3 knockout mice were treated with Aldo for 6 hours or 3 weeks. Aldo increased aortic Gal-3 expression, inflammation, and collagen type I in wild-type mice at both the short-and the long-term, whereas no changes occurred in Gal-3 knock-out mice. Conclusion-Our data indicate that

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mentioning

confidence: 99%

Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

Calvier

Miana

Reboul

et al. 2013

ATVB

326

278

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“…Mac-2 expressing myeloid-lineage cells, including macrophages and dendritic cells, have been shown to produce the B-cell attracting chemokine CXCL13, thus regulating B cell positioning within lymphoid organs. 7,23,24 The percentage of Mac-2 ϩ cells morphologically distinguishable as macrophages and dendritic cells was significantly increased in E-TCL1 Tg ;Rhoh Ϫ/Ϫ spleens (46.7 Ϯ 3.6/ section vs 20.8 Ϯ 1.2; Rhoh Ϫ/Ϫ vs WT, mean Ϯ SEM, P ϭ .004), and pseudofollicles (34.8 Ϯ 7.7/chosen area vs 16.7 Ϯ 3.4; Rhoh Ϫ/Ϫ vs WT; P ϭ .05; supplemental Figure 4B). Therefore the ratio of Rhoh Ϫ/Ϫ CLL cells to accessory cells was also reduced in situ in Rhoh Ϫ/Ϫ spleens.…”

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confidence: 99%

RhoH is critical for cell-microenvironment interactions in chronic lymphocytic leukemia in mice and humans

Troeger

Johnson

Wood

et al. 2012

Blood

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IntroductionIn patients with chronic lymphocytic leukemia (CLL) the characteristic accumulation of monoclonal mature B lymphocytes in the peripheral blood (PB), bone marrow (BM), and secondary lymphoid tissues (SLTs) is mostly attributed to defective in vivo apoptosis, whereas these cells undergo rapid cell death in vitro. 1,2 It has been demonstrated that ex vivo coculture of CLL cells with stromal cells enhances their survival, and a fraction of CLL cells proliferate in close contact with T lymphocytes and stromal cells within pseudofollicles. 3 Therefore, close contact to accessory cells in the BM and SLTs may contribute to their sustained in vivo survival. 2 This is further supported by the observation that CD38 expression associated with adverse outcome in CLL is up-regulated in response to activated T cells, and thus increased in tissues containing pseudofollicles. 4 In long-term in vitro cultures of PB mononuclear cells (PBMNCs) from CLL patients, an adherent cell population, called "nurse-like" cells (NLCs) can be obtained. 5 These NLCs express and produce chemokines, such as CXCL12 and CXCL13, which regulate trafficking of human CLL cells between PB, lymphoid organs, and BM, and thus promote interaction with the microenvironment necessary for their survival and proliferation. 6,7 Furthermore, matrix metalloproteinase-9 is upregulated in response to integrin, CXCL12, and CCR7 signaling via Erk activation in CLL cells and regulates migration and lymph node infiltration thereby contributing to disease progression. 8 Trafficking, directed migration and homing are complex processes that involve the coordinate activation of Rho GTPases, such as Rac and RhoA downstream of integrins, and chemokine receptors in lymphocytes. 9 Their activity varies in a cell and agonist-specific fashion and is dependent in part on their intracellular localization. 10 In this regard, the Src nonreceptor tyrosine kinase and its target focal adhesion kinase (FAK) are critical regulators of both RhoA and Rac. 11 RhoH, a hematopoietic-specific member of the RhoE/Rnd3 subfamily of GTPases was initially identified as hypermutable gene and translocation partner in human B-cell lymphomas suggesting its involvement in the pathogenesis of B-cell malignancies. [12][13][14][15] Rhoh Ϫ/Ϫ mice exhibit a profound T-cell defect because of impaired T-cell receptor (TCR)-mediated selection and maturation of thymocytes as RhoH is required for CD3 phosphorylation and recruitment of the protein tyrosine kinases Zap70 and Lck to the cellular membrane and immunologic synapse. [16][17][18][19] Although the functional importance of RhoH has been well defined in T cells, its role in B-cell development appears less clear. However, in human CLL samples RhoH expression correlates with expression of the unfavorable prognostic marker Zap70. We previously reported an attenuated disease onset in the absence of RhoH in an E-TCL1 Tg mouse model of CLL, 20 which seemed paradoxical given the lack of RhoH involvement in normal B-cell development and the severe T-cel...

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“…HL.2; American Type Culture Collection, USA) and used at a concentration of 1 µg/mL for immunohistochemistry. This antibody has been used to detect galectin-3 in various animal tissues, including mouse tissues [9]. Rabbit anti-ionized calcium binding adapter 1 (Iba-1) (Wako Chemical Pure Industry, Japan) and mouse anti-glial fibrillary acidic protein (GFAP) (Sigma, Spain) were used for the identification of microglia and astrocytes, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Galectin-3 is a β-galactoside-binding animal lectin that is found in a variety of tissues including the immune system in normal mice [9] and is associated with several biological functions including cell adhesion, signaling, proliferation, differentiation, and apoptosis [7], depending on its localization. Intracellular galectin-3 plays a role in cell survival, whereas extracellular galectin-3 mediates cell migration and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical localization of galectin-3 in the brain with Theiler's murine encephalomyelitis virus (DA strain) infection

Shin¹,

Carrillo‐Salinas²,

Martinez³

et al. 2013

Korean Journal of Veterinary Research

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: Galectin-3 is a β-galactoside-binding lectin that plays a role in neuroinflammation through cell migration, proliferation, and apoptosis. In the present study, regulation of galectin-3 was examined in the brain of mice infected with the Daniel strain of Theiler's murine encephalomyelitis virus (TMEV) at days 7 and 81 post-infection by immunohistochemistry. Immunohistochemistry revealed that galectin-3 was mainly localized in ionized calcium-binding adapter 1-positive macrophages/activated microglia, but not in Iba-1-positive ramified microglia. Galectin-3 was also weakly detected in some astrocytes in the same encephalitic lesions, but not in neurons and oligodendrocytes. Collectively, the present findings suggest that galectin-3, mainly produced by activated microglia/macrophages, may be involved in the pathogenesis of virus induced acute inflammation in the early stage as well as the chronic demyelinating lesions in Daniel strain of TMEV induced demyelination model.

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Expression and immunohistochemical localization of galectin‐3 in various mouse tissues

Cited by 100 publications

References 15 publications

Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

RhoH is critical for cell-microenvironment interactions in chronic lymphocytic leukemia in mice and humans

Immunohistochemical localization of galectin-3 in the brain with Theiler's murine encephalomyelitis virus (DA strain) infection

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