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Ayu macrophages at 3.5 hours, 0, 0.5 or 5 ug/ml Leukocyte cell-derived chemotaxin 2 (LECT2), gene expression array, three independent biological replicates

ABSTRACT: Ayu, Plecoglossus altivelis, is an economically important amphidromous fish species cultured in East Asia. LECT2 is a liver derived cytokine and involved in many pathologic conditions, especially in immune regulation. To understand cellular and molecular mechanisms of LECT2 in immune response of ayu, macrophages were isolated from ayu head kidney. After treatment with 0, 0.5 or 5 μg/ml of LECT2 for 3.5 hour, gene expression profile in ayu macrophages was measured using gene expression array. Results showed that LECT2 treatment led to the altered expression of immune related genes in ayu macrophages.

ORGANISM(S): Plecoglossus altivelis

PROVIDER: GSE40221 | GEO | 2012/08/21

SECONDARY ACCESSION(S): PRJNA173221

REPOSITORIES: GEO

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Ayu macrophages at 3.5 hours, 0, 0.5 or 5 ug/ml Leukocyte cell-derived chemotaxin 2 (LECT2), gene expression array, three independent biological replicates

Project description:Ayu, Plecoglossus altivelis, is an economically important amphidromous fish species cultured in East Asia. LECT2 is a liver derived cytokine and involved in many pathologic conditions, especially in immune regulation. To understand cellular and molecular mechanisms of LECT2 in immune response of ayu, macrophages were isolated from ayu head kidney. After treatment with 0, 0.5 or 5 ?g/ml of LECT2 for 3.5 hour, gene expression profile in ayu macrophages was measured using gene expression array. Results showed that LECT2 treatment led to the altered expression of immune related genes in ayu macrophages. Gene expression in ayu macrophages isolated from head kidney were measured after exposure to 0, 0.5 or 5 ?g/ml LECT2 for 3.5 hours using gene expression array. Three independent experiments were performed using different ayu for each experiment for gene expression array analysis.

2012-08-21 | E-GEOD-40221 | biostudies-arrayexpress

Mouse peritoneal macrophages at 3.5 or 48 hours, 0,0.5 or 5 μg/ml Leukocyte cell-derived chemotaxin 2 (LECT2),gene expression array, two independent biological replicates

2011-12-13 | GSE33721 | GEO

Mouse peritoneal macrophages at 3.5 or 48 hours, 0,0.5 or 5 μg/ml Leukocyte cell-derived chemotaxin 2 (LECT2),gene expression array, two independent biological replicates

Project description:LECT2 is a liver derived cytokine and involved in many pathologic conditions, especially in immune regulation. To better understand cellular and molecular mechanisms of LECT2 in immune response, mouse peritoneal macrophages were isolated from mouse peritonaeum. After treatment with 0, 0.5 or 5 μg/ml of LECT2 for 3.5 or 48 hours, gene expression profile in mouse peritoneal macrophages was measured using gene expression array. Results showed that LECT2 treatment led to the enhancement of cytokines secretion and phagocytosis in peritoneal macrophages. Gene expression in mouse peritoneal macrophages isolated from mouse peritonaeum were measured after exposure to 0,0.5 or 5 μg/ml LECT2 for 3.5 or 48 hours using gene expression array. Two independent experiments were performed using different mice for each experiment for gene expression array analysis.

2011-12-13 | E-GEOD-33721 | biostudies-arrayexpress

LECT2 effect on the bone marrow cells of mice

Project description:Hematopoietic stem cell (HSC) is under dynamic controlled in the bone marrow to differentiate into cells of all lineages that constitute the blood. The bone marrow niches form a specific microenvironment to maintain and regulate HSC. However, the mechanisms that the effect of cytokines from blood on HSC function still remain largely unknown. Leukocyte chemotactic factor 2 (LECT2), a liver-derived cytokine, is involved in many immune dysfunctions, such as sepsis, cancer and diabetes. Here we showed that LECT2 affected the gene expression of bone marrow cells in mice. Especially, we found that LECT2 treatment for 3 and 5 days led to the down-regulation of cytokines such as, TNF, IL-6, IL-1β, CXCL10, CCL4, CCL3 et al. Moreover, the functions and mechanisms for LECT2 regulated HSC in bone marrow is still needed further investigation.

2016-05-20 | GSE70014 | GEO

Transcriptional profile comparing murine monocytes infiltrating HCC tumors in the absence/presence of LECT2 expression in the liver

Project description:The aim of this project is to determine the differential expression of genes between monocytes infiltrating HCC nodules in the absence versus in the presence of LECT2

2018-08-13 | GSE99569 | GEO

Transcriptional profile comparing poorly diffentiated HCC nodules to well-differentiated HCC nodules arising in HCC/LECT2-KO mice

Project description:The aim of this project is to determine the differential expression of genes between poorly differntiated HCC tumor compared to differntiated tumor arising in HCC/LECT2-KO mice

2018-08-13 | GSE99568 | GEO

Leukocyte chemotactic factor 2 (LECT2)-associated renal amyloidosis: a case series.

Project description:Renal amyloidosis is characterized by the pathologic deposition within glomeruli and/or interstitium of congophilic fibrils, most often composed of either immunoglobulin light chains or serum amyloid A-related protein and, less commonly, mutated forms of apolipoproteins AI or AII, lysozyme, fibrinogen, gelsolin, or transthyretin.Case series.10 patients with renal amyloidosis who had an amyloidogenic protein that was not identified using routine immunohistochemistry.Clinical, pathologic, biochemical, and genetic characteristics.Tandem mass spectrometry was used to analyze fibrils extracted from sections of formalin-fixed paraffin-embedded amyloid-containing kidney biopsy specimen blocks.Chemical analyses showed peptides corresponding to the carboxy-terminal portion of the leukocyte chemotactic factor 2 (LECT2) molecule. In addition, deposits were immunostained using an anti-human LECT2 monoclonal antibody. Plasma specimens were available from 2 individuals for whom LECT2 concentration in these samples was within the reference range. Additionally, in 4 of the cases analyzed at the molecular level, isolation of genomic DNA and polymerase chain reaction amplification of LECT2-encoding exons showed no mutations. However, all were homozygous for the G allele encoding valine at position 40 in the mature protein, a finding confirmed using restriction enzyme analysis of the polymorphic site.Causality is not addressed.Based on our studies, we posit that LECT2-associated renal amyloidosis represents a unique and perhaps not uncommon disease, especially in Mexican Americans. The pathogenesis, extent, and prognosis remain to be determined.

| S-EPMC2991509 | biostudies-literature

Crystallization and preliminary X-ray analysis of human leukocyte cell-derived chemotaxin 2 (LECT2).

Project description:Human leukocyte cell-derived chemotaxin 2 (LECT2) is a chemotactic factor for neutrophils that plays multifunctional roles in liver regeneration, regulation of neuritic development and proliferation of chondrocytes and osteoblasts. In addition, the C-terminal region of LECT2 belongs to the zinc metalloendopeptidase M23 (PF01551) family. Purified LECT2 was crystallized using the sitting-drop vapour-diffusion method at 293?K. Crystals of selenomethionine-substituted LECT2 that diffracted X-rays to 1.94?Å resolution were obtained using a reservoir solution consisting of 0.2?M ammonium sulfate, 0.1?M HEPES pH 7.5, 25%(w/v) PEG 8000. The crystal belonged to space group P2?2?2?, with unit-cell parameters a=59.4, b=63.5, c=64.0?Å. The calculated Matthews coefficient (VM=2.10?Å3?Da(-1), solvent content 40%) indicates that the crystal consists of two molecules per asymmetric unit.

| S-EPMC3606582 | biostudies-literature

Association of leukocyte cell-derived chemotaxin 2 (LECT2) with NAFLD, metabolic syndrome, and atherosclerosis.

Project description:ObjectivePrevious studies have shown that leukocyte cell-derived chemotaxin 2 (LECT2), a recently discovered hepatokine, is associated with the inflammatory response and insulin resistance. We examined circulating plasma LECT2 levels in the subjects with non-alcoholic fatty liver disease (NAFLD) or metabolic syndrome.MethodsWe analyzed plasma LECT2 levels from the subjects of age- and sex-matched 320 adults with or without NAFLD who completed a health check-up at the Health Promotion Center of Korea University Guro Hospital.ResultsIndividuals with NAFLD showed significantly higher LECT2 levels (31.2 [20.9, 41.5] vs. 24.5[16.3, 32.7] ng/ml, P <0.001) as well as components of MetS compared to those without NAFLD. Furthermore, circulating LECT2 concentrations were greater in subjects with MetS (32.6 [17.8, 45.0] vs. 27.0 [18.7, 33.7] ng/ml, P = 0.016) and were associated with anthropometric measures of obesity, lipid profiles, high sensitivity C-reactive protein (hsCRP) and liver aminotransferase levels. However, there was no significant relationship between LECT2 levels and indicators of subclinical atherosclerosis, such as carotid intima-media thickness (CIMT) and brachial ankle pulse wave velocity (baPWV). Multivariate analysis demonstrated a progressively increasing trend of odds ratios for NAFLD according to quartiles of LECT2 levels after adjusting for risk factors, although the relationship was attenuated after further adjustment for waist circumference and lipid levels.ConclusionCirculating LECT2 concentrations were increased in individuals with NAFLD and those with MetS, but not in those with atherosclerosis. The relationship between LECT2 and both NAFLD and MetS might be mediated by its association with abdominal obesity and lipid metabolism.Trial registrationClinicaltrials.gov NCT01594710.

| S-EPMC5380318 | biostudies-literature

Loss of bound zinc facilitates amyloid fibril formation of leukocyte-cell-derived chemotaxin 2 (LECT2).

Project description:Aggregation of the circulating protein leukocyte-cell-derived chemotaxin 2 (LECT2) causes amyloidosis of LECT2 (ALECT2), one of the most prevalent forms of systemic amyloidosis affecting the kidney and liver. The I40V mutation is thought to be necessary but not sufficient for ALECT2, with a second, as-yet undetermined condition being required for the disease. EM, X-ray diffraction, NMR, and fluorescence experiments demonstrate that LECT2 forms amyloid fibrils in vitro in the absence of other proteins. Removal of LECT2's single bound Zn2+ appears to be obligatory for fibril formation. Zinc-binding affinity is strongly dependent on pH: 9-13 % of LECT2 is calculated to exist in the zinc-free state over the normal pH range of blood, with this fraction rising to 80 % at pH 6.5. The I40V mutation does not alter zinc-binding affinity or kinetics but destabilizes the zinc-free conformation. These results suggest a mechanism in which loss of zinc together with the I40V mutation leads to ALECT2.

| S-EPMC8039541 | biostudies-literature

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