Dataset: Transcription profiling of mouse MH-S cell line with methylglyoxal induces apoptosis and immune response

Mycobacteria-induced apoptosis of macrophages plays an important role in modulation of the host immune response involving TNF-alpha as major cytokine. The underlying mechanisms are still ill-defined. Here, we show for the first time that methylglyoxal (MG) and AGEs levels were elevated during mycobacterial infection of macrophages and that their increased levels mediated mycobacteria-induced apoptotic and immune response of macrophages. Moreover, we show that high levels of AGEs were formed at the sites of pulmonary tuberculosis. This observation represents the first evidence of the potential involvement of AGEs in tuberculosis and in infectious diseases in general. Global gene expression profiling of MG-treated macrophages reveals diversified potential roles of MG in cellular processes, including apoptosis, immune response, and growth regulation. The results of this study provide new insights into intervention strategies to develop therapeutic tools against infectious diseases in which MG and AGE production plays critical roles. Experiment Overall Design: MH-S cells (ATCC Number: CRL-2019), an alveolar macrophage cell line, was treated with 0.8 mM MG. At different time points after treatment (30 min, 4 h, and 8 h) the cells were harvested for total RNA preparation. As negative control the cells without treatment were included. RNA preparation was performed using Trizol method. Totally three independent experiments were performed, so that each time point consists of biological triplicates.

Species:

mouse

Samples:

12

Source:

E-GEOD-3837

PubMed:

17183656

Updated:

Dec.12, 2014

Registered:

Nov.12, 2014