Biomedical subjects

Huan-Yuan Chen

Publications and source records attributed to Huan-Yuan Chen.

4 recordsLinked to original sources

PubMed2006

Role of galectin-3 in mast cell functions: galectin-3-deficient mast cells exhibit impaired mediator release and defective JNK expression.

Galectin-3 is a member of the beta-galactoside-binding animal lectin family expressed in various cell types, including mast cells. To determine the role of galectin-3 in the function of mast cells, we studied bone marrow-derived mast cells (BMMC) from wild-type (gal3(+/+)) and galectin-3-deficient (gal3(-/-)) mice. Cells from the two genotypes showed comparable expression of IgE receptor and c-Kit. However, upon activation by FcepsilonRI cross-linkage, gal3(-/-) BMMC secreted a significantly lower amount of histamine as well as the cytokine IL-4, compared with gal3(+/+) BMMC. In addition, we found significantly reduced passive cutaneous anaphylaxis reactions in gal3(-/-) mice compared with gal3(+/+) mice. These results indicate that there is a defect in the response of mast cells in gal3(-/-) mice. Unexpectedly, we found that gal3(-/-) BMMC contained a dramatically lower basal level of JNK1 protein compared with gal3(+/+) BMMC, which is probably responsible for the lower IL-4 production. The decreased JNK1 level in gal3(-/-) BMMC is accompanied by a lower JNK1 mRNA level, suggesting that galectin-3 regulates the transcription of the JNK gene or processing of its RNA. All together, these results point to an important role of galectin-3 in mast cell biology.

Anaphylaxis↗

PubMed2006

Cell mechanics using atomic force microscopy-based single-cell compression.

We report herein the establishment of a single-cell compression method based on force measurements in atomic force microscopy (AFM). The high-resolution bright-field or confocal laser scanning microscopy guides the location of the AFM probe and then monitors the deformation of cell shape, while microsphere-modified AFM probes compress the cell and measure the force. Force and deformation profiles of living cells reveal a cubic relationship at small deformation (<30%), multiple peaks at 30-70% compression, and a rapid increase at over 80% deformation. The initial compression may be described qualitatively and quantitatively using a simple model of a nonpermeable balloon filled with incompressible fluid. Stress peaks reflect cell membrane rupture, followed by the deformation and rupture of intracellular components, beyond which the cell responses become irreversible. The Young's modulus and bending constant of living cell membranes are extracted from the balloon models, with 10-30 MPa and 17-52 kT, respectively. The initial compression of dead and fixed cells is modeled using Hertzian contact theory, assuming that the cell is a homogeneous sphere. Dead cells exhibit a cytoskeleton elasticity of 4-7.5 kPa, while fixation treatment leads to a dramatic increase in the cytoskeletal Young's modulus (150-230 kPa) due to protein cross-linking by imine bonds. These results demonstrate the high sensitivity of the single-cell compression method to the molecular-level structural changes of cells, which suggests a new generic platform for investigating cell mechanics in tissue engineering and cancer research.

Cell Shape↗

PubMed2004

Galectin-12 is required for adipogenic signaling and adipocyte differentiation.

Galectin-12 is a member of the galectin family consisting of beta-galactoside-binding proteins with conserved carbohydrate recognition domains. This protein is preferentially expressed in peripheral blood leukocytes and adipocytes. We previously showed that galectin-12 is induced by cell cycle block at the G(1) phase and causes G(1) arrest when overexpressed (Yang, R.-Y., Hsu, D. K., Yu, L., Ni, J., and Liu, F.-T. (2001) J. Biol. Chem. 276, 20252-20260). Here, we show that the galectin-12 gene is expressed in mouse preadipocytes and is up-regulated when preadipocytes undergo cell cycle arrest, concomitant with acquisition of the competence to undergo differentiation in response to adipogenic hormone stimulation. Following a brief down-regulation 1 day after adipogenic treatment, its expression was once again markedly elevated when cells underwent terminal differentiation. Down-regulation of endogenous galectin-12 expression by RNA interference greatly reduced the expression of the adipogenic transcription factors CCAAT/enhancer-binding protein-beta and -alpha and peroxisome proliferator-activated receptor-gamma and severely suppressed adipocyte differentiation as a result of defective adipogenic signaling. We conclude that galectin-12 is required for signal transduction that conveys hormone stimulation to the induction of adipogenic factors essential for adipocyte differentiation. The findings suggest that galectin-12 is a major regulator of adipose tissue development.

3T3 Cells↗

PubMed2004

Critical role for galectin-3 in airway inflammation and bronchial hyperresponsiveness in a murine model of asthma.

Galectin-3 is a member of a beta-galactoside-binding animal lectin family. Previous in vitro studies have demonstrated that galectin-3 is involved in a number of activities; however, the roles of this lectin in physiological and pathological processes in vivo remain to be elucidated. Herein, we show, in a murine model of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts of galectin-3; 2) bronchoalveolar lavage fluid from OVA-challenged mice contained significantly higher levels of galectin-3 compared to control mice; and 3) macrophages in bronchoalveolar lavage fluid were the major cell type that contained galectin-3. We investigated the role of galectin-3 in the allergic airway response by comparing galectin-3-deficient (gal3(-/-)) mice and wild-type (gal3(+/+)) mice. OVA-sensitized gal3(-/-) mice developed fewer eosinophils and lower goblet cell metaplasia, after airway OVA challenge compared to similarly treated gal3(+/+) mice. In addition, the OVA-sensitized gal3(-/-) mice developed significantly less airway hyperresponsiveness after airway OVA challenge compared to gal3(+/+) mice. Finally, gal3(-/-) mice developed a lower Th2 response, but a higher Th1 response, suggesting that galectin-3 regulates the Th1/Th2 response. We conclude that galectin-3 may play an important role in the pathogenesis of asthma and inhibitors of this lectin may prove useful for treatment of this disease.

Animals↗