7 results on '"Wang, Min-Cheng"'
Search Results
2. Overexpression of an Outer Membrane Protein Associated with Decreased Susceptibility to Carbapenems in Proteus mirabilis.
- Author
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Tsai, Yi-Lin, Wang, Min-Cheng, Hsueh, Po-Ren, Liu, Ming-Che, Hu, Rouh-Mei, Wu, Yue-Jin, and Liaw, Shwu-Jen
- Subjects
- *
MEMBRANE proteins , *GENE expression , *CARBAPENEMS , *REVERSE transcriptase polymerase chain reaction , *CLINICAL trials - Abstract
Proteus mirabilis isolates commonly have decreased susceptibility to imipenem. Previously, we found P. mirabilis hfq mutant was more resistant to imipenem and an outer membrane protein (OMP) could be involved. Therefore, we investigated the role of this OMP in carbapenem susceptibility. By SDS-PAGE we found this OMP (named ImpR) was increased in hfq mutant and LC-MS/MS revealed it to be the homologue of Salmonella YbfM, which is a porin for chitobiose and subject to MicM (a small RNA) regulation. We demonstrated that ImpR overexpression resulted in increased carbapenem MICs in the laboratory strain and clinical isolates. Chitobiose induced expression of chb (a chitobiose utilization operon). Real-time RT-PCR and SDS-PAGE were performed to elucidate the relationship of hfq, impR, chb and MicM in P. mirabilis. We found MicM RNA was decreased in hfq mutant and chbBC-intergenic region (chbBC-IGR) overexpression strain (chbIGRov), while impR mRNA was increased in hfq mutant, micM mutant and chbIGRov strain. In addition, mutation of hfq or micM and overexpression of chbBC-IGR increased ImpR protein level. Accordingly, chitobiose made wild-type have higher levels of ImpR protein and are more resistant to carbapenems. Hfq- and MicM-complemented strains restored wild-type MICs. Mutation of both impR and hfq eliminated the increase in carbapenem MICs observed in hfq mutant and ImpR-complementation of hfq/impR double mutant resulted in MICs as hfq mutant, indicating that the ImpR-dependent decreased carbapenem susceptibility of hfq mutant. These indicate MicM was antisense to impR mRNA and was negatively-regulated by chbBC-IGR. Together, overexpression of ImpR contributed to the decreased carbapenem susceptibility in P. mirabilis. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
3. The RNA Chaperone Hfq Is Involved in Stress Tolerance and Virulence in Uropathogenic Proteus mirabilis.
- Author
-
Wang, Min-Cheng, Chien, Hsiung-Fei, Tsai, Yi-Lin, Liu, Ming-Che, and Liaw, Shwu-Jen
- Subjects
- *
MOLECULAR chaperones , *STRESS tolerance (Psychology) , *BACTERIAL RNA , *NON-coding RNA , *URINARY tract infection treatment , *LABORATORY mice , *BURNS & scalds , *BACTERIAL vaccines - Abstract
Hfq is a bacterial RNA chaperone involved in the riboregulation of diverse genes via small noncoding RNAs. Here, we show that Hfq is critical for the uropathogenic Proteus mirabilis to effectively colonize the bladder and kidneys in a murine urinary tract infection (UTI) model and to establish burned wound infection of the rats. In this regard, we found the hfq mutant induced higher IL-8 and MIF levels of uroepithelial cells and displayed reduced intra-macrophage survival. The loss of hfq affected bacterial abilities to handle H2O2 and osmotic pressures and to grow at 50°C. Relative to wild-type, the hfq mutant had reduced motility, fewer flagella and less hemolysin expression and was less prone to form biofilm and to adhere to and invade uroepithelial cells. The MR/P fimbrial operon was almost switched to the off phase in the hfq mutant. In addition, we found the hfq mutant exhibited an altered outer membrane profile and had higher RpoE expression, which indicates the hfq mutant may encounter increased envelope stress. With the notion of envelope disturbance in the hfq mutant, we found increased membrane permeability and antibiotic susceptibilities in the hfq mutant. Finally, we showed that Hfq positively regulated the RpoS level and tolerance to H2O2 in the stationary phase seemed largely mediated through the Hfq-dependent RpoS expression. Together, our data indicate that Hfq plays a critical role in P. mirabilis to establish UTIs by modulating stress responses, surface structures and virulence factors. This study suggests Hfq may serve as a scaffold molecule for development of novel anti-P. mirabilis drugs and P. mirabilis hfq mutant is a vaccine candidate for preventing UTIs. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
4. The RNA Chaperone Hfq Is Involved in Stress Tolerance and Virulence in Uropathogenic Proteus mirabilis.
- Author
-
Wang, Min-Cheng, Chien, Hsiung-Fei, Tsai, Yi-Lin, Liu, Ming-Che, and Liaw, Shwu-Jen
- Subjects
MOLECULAR chaperones ,STRESS tolerance (Psychology) ,BACTERIAL RNA ,NON-coding RNA ,URINARY tract infection treatment ,LABORATORY mice ,BURNS & scalds ,BACTERIAL vaccines - Abstract
Hfq is a bacterial RNA chaperone involved in the riboregulation of diverse genes via small noncoding RNAs. Here, we show that Hfq is critical for the uropathogenic Proteus mirabilis to effectively colonize the bladder and kidneys in a murine urinary tract infection (UTI) model and to establish burned wound infection of the rats. In this regard, we found the hfq mutant induced higher IL-8 and MIF levels of uroepithelial cells and displayed reduced intra-macrophage survival. The loss of hfq affected bacterial abilities to handle H
2 O2 and osmotic pressures and to grow at 50°C. Relative to wild-type, the hfq mutant had reduced motility, fewer flagella and less hemolysin expression and was less prone to form biofilm and to adhere to and invade uroepithelial cells. The MR/P fimbrial operon was almost switched to the off phase in the hfq mutant. In addition, we found the hfq mutant exhibited an altered outer membrane profile and had higher RpoE expression, which indicates the hfq mutant may encounter increased envelope stress. With the notion of envelope disturbance in the hfq mutant, we found increased membrane permeability and antibiotic susceptibilities in the hfq mutant. Finally, we showed that Hfq positively regulated the RpoS level and tolerance to H2 O2 in the stationary phase seemed largely mediated through the Hfq-dependent RpoS expression. Together, our data indicate that Hfq plays a critical role in P. mirabilis to establish UTIs by modulating stress responses, surface structures and virulence factors. This study suggests Hfq may serve as a scaffold molecule for development of novel anti-P. mirabilis drugs and P. mirabilis hfq mutant is a vaccine candidate for preventing UTIs. [ABSTRACT FROM AUTHOR]- Published
- 2014
- Full Text
- View/download PDF
5. Fibronectin and culture temperature modulate the efficacy of an avidin-biotin binding system for chondrocyte adhesion and growth on biodegradable polymers.
- Author
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Tsai, Wei-Bor, Wang, Peng-Yuan, Chang, Yung, and Wang, Min-Cheng
- Published
- 2007
- Full Text
- View/download PDF
6. The RNA chaperone Hfq is involved in stress tolerance and virulence in uropathogenic Proteus mirabilis.
- Author
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Wang MC, Chien HF, Tsai YL, Liu MC, and Liaw SJ
- Subjects
- Amino Acid Sequence, Animals, Bacterial Proteins chemistry, Bacterial Proteins genetics, Base Sequence, Biofilms, Cytokines biosynthesis, DNA Primers, Gene Knockout Techniques, Hydrogen Peroxide metabolism, Male, Mice, Mice, Inbred C57BL, Microscopy, Electron, Scanning, Molecular Chaperones chemistry, Molecular Chaperones genetics, Molecular Sequence Data, Osmotic Pressure, Proteus mirabilis metabolism, Proteus mirabilis physiology, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Sequence Homology, Amino Acid, Urinary Tract metabolism, Bacterial Proteins physiology, Molecular Chaperones physiology, Proteus mirabilis pathogenicity, Urinary Tract microbiology, Virulence physiology
- Abstract
Hfq is a bacterial RNA chaperone involved in the riboregulation of diverse genes via small noncoding RNAs. Here, we show that Hfq is critical for the uropathogenic Proteus mirabilis to effectively colonize the bladder and kidneys in a murine urinary tract infection (UTI) model and to establish burned wound infection of the rats. In this regard, we found the hfq mutant induced higher IL-8 and MIF levels of uroepithelial cells and displayed reduced intra-macrophage survival. The loss of hfq affected bacterial abilities to handle H2O2 and osmotic pressures and to grow at 50 °C. Relative to wild-type, the hfq mutant had reduced motility, fewer flagella and less hemolysin expression and was less prone to form biofilm and to adhere to and invade uroepithelial cells. The MR/P fimbrial operon was almost switched to the off phase in the hfq mutant. In addition, we found the hfq mutant exhibited an altered outer membrane profile and had higher RpoE expression, which indicates the hfq mutant may encounter increased envelope stress. With the notion of envelope disturbance in the hfq mutant, we found increased membrane permeability and antibiotic susceptibilities in the hfq mutant. Finally, we showed that Hfq positively regulated the RpoS level and tolerance to H2O2 in the stationary phase seemed largely mediated through the Hfq-dependent RpoS expression. Together, our data indicate that Hfq plays a critical role in P. mirabilis to establish UTIs by modulating stress responses, surface structures and virulence factors. This study suggests Hfq may serve as a scaffold molecule for development of novel anti-P. mirabilis drugs and P. mirabilis hfq mutant is a vaccine candidate for preventing UTIs.
- Published
- 2014
- Full Text
- View/download PDF
7. Effects of an avidin-biotin binding system on chondrocyte adhesion and growth on biodegradable polymers.
- Author
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Tsai WB and Wang MC
- Subjects
- Biodegradation, Environmental, Biotinylation, Cell Proliferation, Chondrocytes chemistry, Chondrocytes physiology, Hydrolysis, Lactic Acid chemistry, Polyesters chemistry, Polyglycolic Acid chemistry, Polylactic Acid-Polyglycolic Acid Copolymer, Avidin chemistry, Biotin chemistry, Cell Adhesion, Chondrocytes cytology, Polymers chemistry, Tissue Engineering methods
- Abstract
Cell adhesion to a scaffold is a prerequisite for tissue engineering. Many studies have been focused on enhancing cell adhesion to synthetic materials that are used for scaffold fabrication. In this study, we applied an avidin-biotin binding system to enhance chondrocyte adhesion to biodegradable polymers. Biotin molecules were conjugated to the cell membrane of chondrocytes, and mediated cell adhesion to avidin-coated surfaces. We demonstrated that immobilization of biotin molecules to chondrocyte surfaces enhanced cell adhesion to avidin-coated biodegradable polymers such as poly(L-lactic acid), poly(D,L-lactic acid), and polycaprolactone, compared to the adhesion of normal chondrocytes to the same type of biodegradable polymer. The biotinylated chondrocytes still maintained their proliferation ability. This study showed the promise of applying the avidin-biotin system in cartilage tissue engineering. [diagram in text].
- Published
- 2005
- Full Text
- View/download PDF
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