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PubMed1995

Eosinophils: from low- to high-affinity immunoglobulin E receptors.

Several experimental approaches have been used to identify immunoglobulin (IgE) binding molecules expressed by human eosinophils. After the description that Fc epsilon RII/CD23 identified on eosinophils could participate in IgE binding and IgE-mediated cytotoxicity, Mac2/epsilon binding proteins belonging to the S-type lectin family were also detected on human eosinophils. Anti-Mac2 monoclonal antibodies inhibited eosinophil-dependent cytotoxicity towards parasitic targets. More recently, Fc epsilon RI was demonstrated on human eosinophils from hypereosinophilic patients. The 3 components of Fc epsilon RI, alpha, beta and gamma chains, were detected in eosinophils. The alpha chain of Fc epsilon RI was shown to be involved in IgE binding to eosinophils and in the selective release of eosinophil peroxidase. The participation of Fc epsilon RI-bearing eosinophils in a protective immune response against a parasitic infection indicates a so far unsuspected function of Fc epsilon RI. The interactions between the different types of IgE binding molecules are discussed.

Antigens, Differentiation↗

PubMed1994

Expression of Mac-2 antigen in the preosteoclast and osteoclast identified in the op/op mouse injected with macrophage colony-stimulating factor.

Osteoclast deficiency in op/op mice is cured by a single injection of 5 micrograms recombinant human macrophage colony-stimulating factor (rhM-CSF). In this study, we found that mouse osteoclasts are positive for Mac-2 antigen, but not for F4/80, MOMA-2, Mac-1, or BM8 antigen. By using F4/80 and MOMA-2 monoclonal antibodies, we confirmed the absence of mature macrophages in the femora of op/op mice and found that multiple injections of rhM-CSF are required for the recruitment of macrophages in the bones. After a single rhM-CSF injection, we found Mac-2 positive mononuclear cells in the femora of op/op mice. The time course of the appearance of Mac-2-positive cells was very similar to that of tartrate-resistant acid phosphatase (TRAP)-positive cells. In bone sections prepared from the mutant mice that received rhM-CSF 3 days earlier, 91% of the TRAP-positive mononuclear cells were also positive for Mac-2 antigen. These results demonstrate the expression of Mac-2 antigen in preosteoclasts. The antigen was detected on the plasma membrane of preosteoclasts, as well as in their cytoplasm and nucleus, and in the extracellular matrix in the space between the cells and bone. Since Mac-2 is a galactose-specific lectin, a potential role of the lectin in cell-cell and cell-matrix adhesion during osteoclast differentiation is suggested.

Animals↗

PubMed1993

Compartmentalized reactivity of M3/38 (anti-Mac-2) and M3/84 (anti-Mac-3) in the uterus of pregnant mice.

Changes in the expression of antigens on mouse uterine or embryonic tissues were examined by enzyme immunocytochemistry. Cryostat sections of uteri from days 1, 8 and 15 of pregnancy were probed with the monoclonal antibodies M3/38 and M3/84, originally defined by their reactivity with macrophage surface antigens (Mac-2 and Mac-3, respectively). In the uterus of pregnant mice, reaction of these antibodies was not limited to leucocytes. M3/38 did not react at detectable levels with cells in the uterus on day 1 but did react with decidual cells immediately surrounding the embryo on day 8. By day 15, the placenta, decidua basalis and metrial gland were intensely positive but the embryo was negative. M3/84 reacted with the luminal side of the endometrium on day 1, the entire decidual mass on day 8, and with all maternal and fetal tissues on day 15. M3/38 was detected in saline-soluble preparations of uterine tissue and had a molecular mass of approximately 32-35 kDa as determined by SDS-PAGE and western blot analysis. The pattern of expression of these molecules suggests a functional relationship to developmental changes that occur at the maternal-fetal interface.

Animals↗

PubMed1989

Increased production of cytotoxic macrophage progenitors by Lactobacillus casei in mice.

Heat-killed Lactobacillus casei YIT9018 (LC9018), when administered intravenously to normal mice, induced increase in Mac-1+ cells and Mac-2+ cells but not in Mac-3+ cells in spleen. The number of both populations changed in the same time course and was maximal 14 d after the administration. To know the effect of LC9018 on hematopoietic progenitor level, we examined the number of macrophage colony-forming cells (M-CFC), granulocyte-macrophage CFC (GM-CFC), and colony-forming units in spleen (CFU-S) in bone marrow 3 d after the administration. LC9018 stimulated the proliferation of M-CFC but not that of GM-CFC and CFU-S. LC9018-induced M-CFC were similar to normal M-CFC in dependence on macrophage colony-stimulating factor (M-CSF) and buoyant density. M-CFC-derived macrophages cultured in the presence of M-CSF expressed Mac-1 and Mac-2 but not Mac-3. They showed cytotoxic activity against syngenic tumor cells, Meth A, via direct contact, when assayed by using an in vitro colony inhibition assay or an in vivo Winn test. These results indicate that LC9018 stimulates the proliferation of cytotoxic macrophage progenitors in bone marrow and induces their differentiation in spleen. These effects may be one of the ways in which LC9018 suppresses tumor growth.

Adjuvants, Immunologic↗

PubMedDate not supplied

Cross-reactivity between IgE-binding proteins from Anisakis simplex and Dermatophagoides pteronyssinus.

An association was found between Anisakis simplex (As) and Dermatophagoides pteronyssinus (Dp) sensitization. One recent study shows a cross-reactivity between As and Dp and tropomyosin (tr)is suspected as being one of the proteins responsible of this cross-reaction. The aim of our study was: 1) to confirm the cross-reactivity between Dp and As; 2) to determine the importance of tr in this cross reaction. SDS-PAGE analysis of Dp and As (metabolic and somatic) extracts was carried out. Then an IgE immunoblotting test using serum from a patient who had specific IgE only to Dp and As and immunoblotting inhibition experiments using Dp extract and tr as inhibitors were performed. We found that patients serum reacted: 1) against larval As antigens with a molecular weight (mw) of 25 kilodalton (kD) and a mw > than 100 kD, 2) against various metabolic As antigens with a mw > than 100 kD, a mw ranging approximately from 35 to 50 kD, and a mw around 20 kD, and 3) against Dp proteins with mw between 35 and 55 kD. Preincubation of patient's serum with Dp extract caused the disappearance of reactivity against antigens with a mw > than 100 kD in both larval and metabolic As extracts and against proteins with mw ranging approximately from 35 to 50 kD in the metabolic As extract. Preincubation of patients serum with As extract caused the disappearance of reactivity against antigens with mw between 35 and 55 kD in the Dp extract. Pre-incubation of patients serum with tr did not induce any change in the immunoblotting profile. The results show that 1) cross-reactive components between Dp and As are some proteins with a mw ranging approximately from 35 to 50 kD and with a mw > than 100 kD, and 2) tr is not involved in cross-reactivity between As and Dp.

Adult↗

PubMed1991

The role of tumor-derived cytokines on the immune system of mice bearing a mammary adenocarcinoma. I. Induction of regulatory macrophages in normal mice by the in vivo administration of rGM-CSF.

Using a dimethylbenzanthracene-induced immunogenic nonmetastatic murine mammary adenocarcinoma in BALB/c mice, our previous work has shown that splenocytes from tumor bearers have reduced responses to both mitogens and Ag including tumor-associated Ag. NK and cytotoxic T cell activities are also reduced in splenocytes of tumor bearers. Mac-1+2+ macrophages induced in mammary tumor bearers are capable of down-regulating lymphocyte responses to mitogens and tumor-associated Ag by cell to cell contact interaction and increased PGE2 production. We have found that the tumor constitutively releases a granulocyte-macrophage (GM)-CSF-like factor in vivo and in vitro, which may be responsible for the systemic increase in cells of the macrophage lineage in tumor-bearing mice. A tumor cell line established from the in vivo tumor expresses and releases GM-CSF as shown by Northern and Western blot analyses. Daily i.p. injections for 3 wk of 10,000 U of rGM-CSF into normal mice induces hemopoietic and immunologic alterations similar to those observed in tumor bearers. Mac-1+ and/or Mac-2+ macrophages can also be detected in the spleens and bone marrow of the mice treated with rGM-CSF. Additionally, splenocytes from rGM-CSF-treated mice have reduced responses to mitogens and their peritoneal exudate cells can cause in vitro down-regulation of proliferative responses of lymphocytes from normal mice. The suppression can be partially reversed by the addition of indomethacin to the cultures suggesting that PGE2 may contribute to the effect. rGM-CSF enhances the in vitro release of PGE2 by the spleen, bone marrow, and peritoneal cells of normal mice. These data indicate that the high levels of GM-CSF constitutively produced by the tumor may be responsible for the hemopoietic changes and immunologic alterations observed in tumor-bearing mice.

Adenocarcinoma↗

PubMed1993

Normal development of mice carrying a null mutation in the gene encoding the L14 S-type lectin.

The L14 lectin is a 14 x 10(3) M(r) carbohydrate binding protein belonging to the family of S-type lectins. The pattern of expression of this protein during mouse embryogenesis suggests that it may have multiple roles during pre- and post-implantation development. Using the technique of homologous recombination in embryonic stem cells, we have introduced a null mutation in the gene encoding the L14 lectin and generated a strain of mice carrying the mutant allele. We report here that homozygous mutant animals that lack the L14 lectin develop normally and are viable and fertile. The absence of any major phenotypic abnormalities in these mutant animals suggests that other protein(s) potentially compensate for the absence of the L14 lectin. Here we show that a related protein termed L30, a lectin that has carbohydrate binding specificity similar to that of L14, is present in the same embryonic cell populations as L14 at the time of implantation, suggesting that the two S-type lectins may be capable of functional substitution at this early stage of embryogenesis.

Animals↗

PubMed1991

Splenic macrophages from tumor-bearing mice co-expressing MAC-1 and MAC-2 antigens exert immunoregulatory functions via two distinct mechanisms.

Tumor burden has been shown to induce a variety of phenotypic and functional changes in the cellular constituents of the host's immune system. These changes have been implicated as mechanisms by which tumors avoid rejection. Studies of BALB/c mice bearing a D1-DMBA-3 mammary adenocarcinoma showed alterations of the splenocyte populations. There was a five-fold increase of macrophages (M phi) that were phenotypically and functionally analyzed to establish their role in tumor-induced modifications of the host's immune response. Monoclonal antibody staining defined a Mac-1+2+ population which comprised up to 20% of the splenocytes in tumor-bearers (TB), but is negligible in spleens from normal mice. These Mac-1+2+ M phi were found to mediate down-regulation of both polyclonal and antigen-specific T and B cell responses in vitro and in vivo. Although B cell responses were suppressed via prostaglandin E2 (PGE2) production by the TB M phi, T cell responses were relatively refractory to PGE2-mediated down-regulation. Instead, they were suppressed by a contact-dependent T cell-M phi interaction. Furthermore, tumor-derived factors such as granulocyte-M phi colony-stimulating factor (GM-CSF) seem to play an important role in the induction and expansion of the Mac-1+2+ M phi. These cells appear to mediate down-regulation of the host immune responses by at least two distinct mechanisms: 1) PGE2 production and 2) a cell contact-dependent, but non-major-histocompatibility-complex-specific, interaction.

Adenocarcinoma↗

PubMed2006

Differential allergen sensitization patterns in chestnut allergy with or without associated latex-fruit syndrome.

BACKGROUND: Chestnut allergy has been almost exclusively considered in the context of the latex-fruit syndrome. Chestnut allergens not linked to latex hypersensitivity have not been studied. OBJECTIVE: We sought to explore whether differences in sensitization patterns between chestnut allergy with or without associated latex-fruit syndrome can be detected. METHODS: Twelve patients sensitized to chestnut but not to latex and 3 control patients with latex-chestnut allergy were analyzed. A major chestnut allergen was purified and characterized. IgE immunoblotting, specific IgE determination, and skin prick tests with 5 isolated allergens involved in food allergy or latex-fruit syndrome were also performed. RESULTS: A major 9-kd allergen was detected in chestnut extract, isolated, and identified as lipid transfer protein (LTP) Cas s 8. Specific IgE to this allergen was found in 91% (by means of IgE immunoblotting) and 58% (by means of ELISA) of sera from patients with chestnut but not latex allergy. Moreover, 66% of these patients had positive skin prick test responses to Cas s 8. Additionally, allergenic LTPs from peach fruit and Artemisia vulgaris pollen were also reactive. In contrast, avocado class I chitinase and latex hevein, allergens associated with the latex-fruit syndrome, showed no reaction. The opposite situation was exhibited by patients with latex-chestnut allergy. CONCLUSIONS: Patients with chestnut allergy with or without associated latex hypersensitivity present different patterns of major allergens (LTPs and class I chitinases, respectively). CLINICAL IMPLICATIONS: LTPs and class I chitinases can be used as diagnostic tools in patients with chestnut allergy to predict whether an associated latex sensitization and a risk of potential cross-reactivity with other plant foods and pollens exist.

Adolescent↗

PubMed2001

Glycoprotein 90K/MAC-2BP interacts with galectin-1 and mediates galectin-1-induced cell aggregation.

The glycoprotein 90K was originally described as a tumor-secreted antigen and subsequently found to have immunostimulatory activity as well as other possible functions. This protein interacts with an endogenous lectin, galectin-3, and may play a role in tumor metastasis through this interaction. Because 90K is heavily glycosylated, it may also interact with other members of the galectin family, which would contribute to the multifunctionality of 90K. To test this possibility, we studied the recognition of 90K by galectin-1, which, like galectin-3, has been associated with neoplastic transformation. In a solid-phase binding assay, human recombinant galectin-1 bound immobilized human recombinant 90K in a fashion that was inhibitable by lactose. Galectins 1 and 3 appeared to bind to separate sites on 90K because they did not affect the binding of each other. The dissociation constant of galectin-1 to 90K was on the order of 10(-7) M. Galectin-1 also induced aggregation of a human melanoma cell line, A375, in a carbohydrate-dependent manner, and this appeared to be mediated, at least in part, by 90K expressed on A375 cells, since it was inhibitable by a specific anti-90K monoclonal antibody. We conclude that 90K interacts with both galectin-1 and galectin-3 and both interactions contribute to the formation of multicell aggregates. Because both of these galectins as well as 90K are often over-expressed in neoplasm, these interactions may occur in the setting of various carcinomas and contribute to their progression and metastasis.

3T3 Cells↗

PubMed2003

Expression patterns of galectin-1 and galectin-3 in nasal polyps and middle and inferior turbinates in relation to growth regulation and immunosuppression.

BACKGROUND: The term nasal polyposis describes benign growth processes in the nasal and sinus mucosa, which are mainly located in the middle meatus and never in the inferior meatus. As a step to define the biochemical determinants relevant for growth regulation, we focused on endogenous lectins known for anti-apoptotic (galectin-3) and immunomodulatory (galectin-1) activities. DESIGN: Using computer-assisted microscopy, we performed an immunohistochemical investigation defining the quantitative parameters of expression of galectin-1 and galectin-3 in 10 nasal polyps, 10 middle turbinates, and 10 inferior turbinates, all of which were obtained from surgical resection. RESULTS: Our data show that galectin-3 expression is markedly (P<.001) higher in nasal polyps than in turbinates. No relation to the allergic status was discovered. Galectin-1 expression is higher in nasal polyps than in middle turbinates (P<.001) in nonallergic patients compared with allergic ones (in glandular epithelium, P =.009; in connective tissue, P =.006). The lowest galectin-1 expression was observed in the middle turbinate. CONCLUSIONS: These data are in line with a positive influence of galectin-3 on growth and an immunoregulatory role of galectin-1, mimicking an increased expression dependent on glucocorticoid.

Adjuvants, Immunologic↗

PubMed1991

Carbohydrate-binding protein 35 is the major cell-surface laminin-binding protein in colon carcinoma.

The interaction of tumor cells with laminin is thought to be critical in invasion and metastasis. We found that an endogenous lectin, carbohydrate-binding protein 35 (CBP-35), is the major laminin-binding protein on human colon carcinoma cells and that its surface expression suggests involvement in metastasis. We identified CBP-35 by laminin-affinity chromatography and immunoblotting. Surface expression of CBP-35 on eight human colon carcinoma cell lines was compared by flow cytometry. Poorly differentiated cell lines and DLD-2, a signet-ring carcinoma cell line, expressed more surface CBP-35 than well-differentiated cell lines. Poorly differentiated cell lines and DLD-2 are characterized as aggressive cell lines because they adhere to and invade through reconstituted basement membrane significantly better than well-differentiated cell lines. These data suggest that CBP-35 is involved in tumor cell-basement membrane interactions and that an increase in CBP-35 surface expression may facilitate metastatic potential of colon carcinoma cells.

Antigens, Differentiation↗

PubMed1997

Galectin-3 and laminin expression in neoplastic and non-neoplastic thyroid tissue.

Galectin-3 is a 31 kD beta-galactoside-binding lectin which is expressed by several types of non-neoplastic and neoplastic cells and which may be involved in cell-extracellular matrix interactions. An immunohistochemical study has been made of the expression of galectin-3, as well as its ligand, laminin, in a spectrum of benign and malignant thyroid neoplasms and in some non-neoplastic conditions. Immunohistochemistry with anti-human recombinant galectin-3 antibody showed consistent, intense positivity in the neoplastic cells of 18 cases of papillary carcinoma and less intense staining in the five anaplastic carcinomas studied. In addition, two out of three poorly differentiated carcinomas, three out of six medullary carcinomas, and four out of eight follicular carcinomas had less intense or focal positivity. One case of Hürthle cell carcinoma showed scattered strongly positive cells. Eight follicular adenomas, three hyperplastic nodules, five nodular goitres, and normal thyroid tissue were negative. Galectin-3 mRNA expression was also evaluated in three of the papillary carcinomas, two follicular adenomas, and one hyperplastic nodule with matched normal tissue. Northern blot analysis demonstrated mRNA overexpression in the three cases of papillary carcinomas, whereas normal and benign tissues were negative. Laminin distribution in neoplastic and non-neoplastic tissue varied with architectural patterns but did not correlate with galectin-3 immunohistochemical expression. We conclude that expression of galectin-3 is limited to inflammatory foci in normal and benign thyroid tissue and is a phenotypic feature of malignant thyroid neoplasms, especially papillary carcinomas.

Antigens, Differentiation↗

PubMed1999

Galectin-3 modulates rat mesangial cell proliferation and matrix synthesis during experimental glomerulonephritis induced by anti-Thy1.1 antibodies.

Galectin-3 is a beta-galactoside-binding protein synthesized by macrophages and other inflammatory cells and expressed in various branching epithelia, including the developing kidney. The expression of galectin-3 has been studied in a rat model of acute mesangial proliferative glomerulonephritis in which a single injection of anti-Thy1.1 antibodies leads to destruction of mesangial cells expressing a Thy1.1 epitope on their surface. The glomerular lesion is characterized by expansion of the mesangial matrix, especially laminin and collagen type IV, and mesangial hypercellularity. Galectin-3 expression, which is sparse in mature rat kidney and confined to the apical face of some distal tubules, is increased within 1-3 days following antibody administration, with the recruitment of glomerular macrophages and pronounced neo-expression in the cytoplasm and at the basal face of distal tubules. At later times, galectin-3 is detected immunohistochemically in the repopulating mesangial cell mass, preceding the extensive mesangial deposition of laminin and collagen type IV. Mesangial cells in culture do not produce appreciable amounts of galectin-3 but do bind and endocytose exogenously added lectin. Addition of galectin-3 to primary cultures of mesangial cells prepared from normal rats induces a 1.5-fold increase in the synthesis of collagen type IV and it also acts in synergy with a quantitatively similar stimulatory effect of transforming growth factor beta (TGF-beta) on matrix synthesis. Exogenous galectin-3 prolongs the survival of mesangial cells in serum-free cultures and also protects these cells against cytotoxic effects of TGF-beta. The data support the notion that the increased expression and secretion of galectin-3 in infiltrating macrophages and in distal tubular epithelia, together with up-regulation of IL-1beta and TGF-beta genes, play a role in mesangial hypercellularity in the progression of one model of inflammatory renal disease.

Animals↗

PubMed1998

Mass spectrometric identification and microcharacterization of proteins from electrophoretic gels: strategies and applications.

The entire genomic DNA sequences of a number of prokaryotic and eukaryotic species are now available and many more, including the human genome, will be completed in the near future. The state-of-life of a cell at any given time, however, is defined by its protein composition, i.e., its proteome. Gel electrophoresis, mass spectrometry, and bioinformatics will be important tools for protein and proteome analysis in the post-genome era. Protein identification from electrophoretic gels by mass spectrometric peptide mapping or peptide sequencing combined with sequence database searching is established and has been applied to numerous biological systems. We describe current strategies and selected applications in molecular and cell biology. The next challenges are detailed structure/function analyses, which include studying the molecular composition of multiprotein complexes and characterization of secondary modifications of proteins. The advantages and limitations of a number of mass spectrometry-based strategies designed for microcharacterization of low amounts of protein from electrophoretic gels are discussed and illustrated by examples.

Amino Acid Sequence↗

PubMed1999

The levels of expression of galectin-1, galectin-3, and the Thomsen-Friedenreich antigen and their binding sites decrease as clinical aggressiveness increases in head and neck cancers.

BACKGROUND: The aim of this study was to investigate whether an increase in malignancy level is accompanied by significant modifications of the expression of galectin-1, galectin-3, and Thomsen-Friedenreich antigen (T antigen) as well as the expression of binding sites for these three markers in head and neck squamous cell carcinomas (HNSCCs). METHODS: Immunohistochemical and glycohistochemical staining reactions were carried out with antibodies, labeled lectins, and a custom-made neoglycoprotein on the basis of histologic slides from a retrospective series of 40 normal and 75 HNSCC formalin fixed, paraffin embedded tissues, and were quantitatively described with the aid of computer-assisted microscopy. RESULTS: Whatever the histologic type, the epithelial tissues in HNSCC exhibited very significantly (P < 0.01 to P < 0. 0001) lower amounts of galectin-1, galectin-3, and T antigen and their respective binding sites than their corresponding normal counterparts. The tumors of the larynx differed very significantly (P < 0.0001 to P < 0.000001) from all the other tumor types. A loss of differentiation in the HNSCCs is accompanied first by the loss of expression of galectin-3 and galectin-3-reactive sites and then by that of the T antigen and its binding site(s). The opposite feature was observed when the parameters associated with the TNM classification were taken into account. The negative lymph node HNSCCs could be distinguished (P = 0.02) from the positive lymph node HNSCCs on the basis of a loss of galectin-3 expression. The modifications occurring in the extent of expression of galectin-1 and galectin-1-reactive sites were relatively marginal in comparison with those observed for galectin-3-dependent and T- antigen-dependent staining. CONCLUSIONS: The decrease in the extent of expression of galectin-3 and galectin-3-reactive sites, T antigen and T antigen-binding sites, and, to a lesser extent, galectin-1 and galectin-1-reactive sites correlates significantly with an increasing level of clinically detectable HNSCC aggressiveness.

Adjuvants, Immunologic↗

PubMed1996

Identification and characterization of up-regulated genes during chondrocyte hypertrophy.

Chondrocyte hypertrophy involves de novo acquisition and/or increased expression of certain gene products including, among others, type X collagen, alkaline phosphatase, and matrix metalloproteinases. To analyze further the genetic program associated with chondrocyte hypertrophy, we have employed a modification of the polymerase chain reaction-mediated subtractive hybridization method of Wang and Brown (Wang and Brown [1991] Proc. Natl. Acad. Sci 88:11505). Cultures of hypertrophic tibial chondrocytes and nonhypertrophic sternal cells were used for poly A+ RNA isolation. Among 50 individual cDNA fragments isolated for up-regulated hypertrophic genes, 18 were tentatively identified by their similarities to entries in the GenBank database, whereas the other 32 showed no significant similarity. The identified genes included translational and transcriptional regulatory factors, ribosomal proteins, the enzymes transglutaminase and glycogen phosphorylase, type X collagen (highly specific for hypertrophic cartilage matrix), gelsolin, and the carbohydrate-binding protein galectin. Two of these, transglutaminase and galectin, were cloned and were further characterized. The chondrocyte transglutaminase revealed previously in hypertrophic cartilage by immunochemical methods appears to be the chicken equivalent of mammalian factor XIIIa (showing 75% overall protein similarity). The chicken chondrocyte galectin is a variant of mammalian galectin-3. Galectins are known to bind to components found in hypertrophic cartilage, and factor XIIIa is known to crosslink some of the same components, possibly modifying them for calcification and/or removal.

Amino Acid Sequence↗

PubMed1997

Differential expression of galectin-1 and galectin-3 during first trimester human embryogenesis.

Development of complex organisms requires specific temporospatial differentiation and expression of the correct phenotype through activation of a variety of genes. Galectins are mammalian lectins able to interact with various extracellular matrix glycoconjugates and have been implicated in several biological events including cell attachment, differentiation, apoptosis, embryogenesis, and cancer invasion and metastasis. In this study, we have examined the expression of galectin-1 and galectin-3 during human first trimester embryogenesis using immunohistochemistry and Western blotting. Variable amounts of galectin-1 and galectin-3 were detected in all tissue protein extracts. Galectin-1 expression was demonstrated in the connective tissue and derived tissues such as smooth and striated muscle cells, and in some epithelia, such as in the basal layers of the skin after 14 weeks and in the epithelial cells of the gonads. Galectin-3 was detected mainly in epithelia, such as the skin, epithelial lining of the digestive and respiratory tract, and urothelium and excretory tubes of the kidney, but also in the myocardial cells, in the peripheral and preossifying hypertrophic chondrocytes, and in the notochord and in the liver. Our study constitutes the first demonstration of galectin-1 and galectin-3 during human embryogenesis. The differential expression of these two lectins suggests that they could participate in the complex processes of tissue differentiation.

Antigens, Differentiation↗