Biomedical subjects

Meihong Chen

Publications and source records attributed to Meihong Chen.

4 recordsLinked to original sources

PubMed2006

Rapid identification of small interfering RNA that can effectively inhibit the replication of multiple influenza B virus strains.

Influenza B virus is a cause of substantial morbidity and mortality in humans and current vaccination strategies and antiviral drugs only provide limited protection. Here, we report the evaluation of small interfering RNA (siRNA) for repression of viral replication in cultured cells as well as in chicken embryos. Several siRNAs targeting conserved regions of the virus (in chemically synthesized or plasmid-encoded forms) were found to effectively block the replication of the influenza B virus. The siRNAs were found to offer broad protection over several strains of influenza B virus (B/Beijing/76/98, B/Beijing/37/99 and B/Jiangsu/10/03) that differ substantially in their genetic content. The antiviral effects of 500 ng siRNA-encoding plasmids or 60 nmoles synthetic siRNA were found to be comparable to that of 3.6 microg ribavirin. These results indicated that RNA interference warrants further study for management of influenza B virus infections.

Animals↗

PubMed2005

A universal plasmid library encoding all permutations of small interfering RNA.

Small interfering RNA (siRNA) is normally designed to silence preselected known genes. Such selections are inevitably prone to bias as a result of limited knowledge about the biological process, transcript identity, and functions. A library that contains all permutations of siRNA could avoid such problems. In this paper, it is shown that 5 x 10(7) siRNA-encoding plasmids can be constructed in a single tube by using vectors with two mutated RNA polymerase III promoters arranged in a convergent manner. Such a library was used to carry out genomewide screening of functional genes in a phenotype-driven manner. Multiple siRNAs that induce a significant increase of cell proliferation speed were identified.

Base Sequence↗

PubMed2002

CDK inhibitor p18(INK4c) is required for the generation of functional plasma cells.

B cell terminal differentiation is associated with the onset of high-level antibody secretion and cell cycle arrest. Here the cyclin-dependent kinase (CDK) inhibitor p18(INK4c) is shown to be required within B cells for both terminating cell proliferation and differentiation of functional plasma cells. In its absence, B cells hyperproliferate in germinal centers and extrafollicular foci in response to T-dependent antigens but serum antibody titers are severely reduced, despite unimpaired germinal center formation, class switch recombination, variable region-directed hypermutation, and differentiation to antibody-containing plasmacytoid cells. The novel link between cell cycle control and plasma cell differentiation may, at least in part, relate to p18(INK4c) inhibition of CDK6. Cell cycle arrest mediated by p18(INK4C) is therefore requisite for the generation of functional plasma cells.

Animals↗

PubMed2002

Characterization of a murine model of endotoxin-induced acute lung injury.

Endotoxin-induced microvascular lung injury in mice is a commonly used experimental model of the acute respiratory distress syndrome (ARDS). The present paper aimed to characterize this popular model in a comprehensive and systematic fashion. Male C57bl/6 mice (n = 5) were administered an LD55 dose of E. coli endotoxin (15 mg/kg, i.p.), and lungs were harvested at several time points and evaluated for injury as well as for expression of a variety of inflammatory mediators. Endotoxin induced many features characteristic of acute microvascular lung injury. These included early (1-2 h) expression of inflammatory mediators (IL-1alpha, IL-1beta, IL-4, IL-6, IL-10, TNF-alpha, interferon-alpha, interferon gamma, and MCP-1) and leukocyte accumulation in lung tissue (lung myeloperoxidase activity 18.5 +/- 7.8 U/g tissue, P < 0.05), followed by pulmonary edema (lung water content index 17.4% +/- 2.5%, P < 0.05) and mortality. Histopathological evaluation of lung tissue was compatible with these findings. The characterization of this murine model of endotoxin-induced microvascular injury will facilitate its utilization in ARDS research.

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