Biomedical subjects

Shinn-Jong Jiang

Publications and source records attributed to Shinn-Jong Jiang.

4 recordsLinked to original sources

PubMed2004

Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite.

The effect of arsenite pretreatment on bovine herpesvirus-4 (BHV-4) replication in bovine arterial endothelial (BAE) cells was studied. BHV-4 infectivity, including IE-2 expression, DNA replication and viral yield, were significantly reduced at nontoxic concentrations of arsenite in which cellular DNA synthesis or cell viability of BAE cells were not affected under resting and confluent conditions. This effect was accompanied by the induction of heat shock protein 70 (HSP70) and an interrupted cell cycle (causing cell cultures to accumulate at the S and G2/M phases). Actinomycin D inhibited the induction of HSP70 and reduced arsenite antiviral activity. In conclusion, cellular stress response induced by arsenite in BAE cells inhibited replication of BHV-4, and probably resulted from the induction of HSP70 and interference of cell cycle progression.

Animals↗

PubMed2003

Thrombomodulin-mediated cell adhesion: involvement of its lectin-like domain.

Thrombomodulin (TM) is an integral membrane glycoprotein that is a potent anticoagulant factor. TM may also possess functions distinct from its anticoagulant activity. Here the influence of TM on cell adhesion was studied in TM-negative melanoma A2058 cells transfected with green fluorescent protein-tagged TM (TMG) or lectin domain-deleted TM (TMG(DeltaL)). Confocal microscopy demonstrated that both TMG and TMG(DeltaL) were distributed in the plasma membrane. TMG-expressed cells grew as closely clustered colonies, with TM localized prominently in the intercellular boundaries. TMG(DeltaL)-expressed cells grew singly. Overexpression of TMG, but not TMG(DeltaL), decreased monolayer permeability in vitro and tumor growth in vivo. The cell-to-cell adhesion in TMG-expressed cells was Ca2+-dependent and was inhibited by monoclonal antibody against the lectin-like domain of TM. The effects of TM-mediated cell adhesion were abolished by the addition of mannose, chondroitin sulfate A, or chondroitin sulfate C. In addition, anti-lectin-like domain antibody disrupted the close clustering of the endogenous TM-expressed keratinocyte HaCaT cell line derived from normal human epidermis. Double-labeling immunofluorescence staining revealed similar distributions of TM and actin filament in the cortex region of the TMG-expressed cells. Thus, TM can function as a Ca2+-dependent cell-to-cell adhesion molecule. Binding of specific carbohydrates to the lectin-like domain is essential for this specific function.

Calcium↗

PubMed2002

Decrease of fibrinolytic activity in human endothelial cells by arsenite.

Blackfoot disease (BFD) is an endemic peripheral vascular occlusive disease that occurred in the southwest coast of Taiwan. It is believed that arsenic in the drinking water from artesian wells plays an important role in the development of the disease. We have previously shown that BFD patients had significant lower tissue-type plasminogen activator (t-PA) antigen level and higher plasminogen activator inhibitor, Type 1 (PAI-1) antigen level than normal controls. The purpose of this study was to investigate the effects of arsenite on the fibrinolytic and anticoagulant activities of cultured macrovascular and microvascular endothelial cells. Incubation of human microvascular endothelial cells (HMEC-1), but not human umbilical vein endothelial cells (HUVECs), with arsenite caused a decrease of t-PA mRNA level, a rise of both PAI-1 mRNA level and PAI activity. Arsenite could also inhibit the thrombomodulin (TM) mRNA expression and reduce the TM antigen level in HMEC-1. In conclusion, arsenite had a greater effect on HMEC-1 as compared to HUVECs in lowering the fibrinolytic activity and may be responsible for the reduced capacity of fibrinolysis associated with BFD.

Arsenites↗

PubMedDate not supplied

Inhibition of bovine herpesvirus-4 replication by arsenite through downregulation of the extracellular signal-regulated kinase signaling pathway.

Infection of bovine arterial endothelial (BAE) cells with bovine herpesvirus-4 (BHV-4) induced biphasic activation of one of the cellular mitogen-activated protein kinase (MAPK) downstream targets, extracellular signal-regulated kinase (ERK). ERK activity reached a maximum within 0.5 h postinfection (h.p.i.), and had declined and returned to basal levels by 2 h.p.i. However, at 18- 24 h.p.i., a second phase of increased ERK activation occurred. Treatment of BHV-4-infected BAE cells with either U0126, a potent inhibitor of MAPK/ERK kinase, or arsenite dose-dependently blocked ERK activation and inhibited viral DNA synthesis and viral replication in the culture. Further detailed investigations revealed that transcription of viral immediate-early gene 2 (IE-2), which is required for viral DNA replication, was significantly suppressed by both U0126 and arsenite. These results imply that ERK activation may play a pivotal role in herpesvirus replication, and that inhibition of ERK activation can effectively inhibit viral IE protein synthesis and viral replication.

Animals↗