sodium-dodecyl-sulfate and Hypoxia

The mce4 operon is one of the four mce operons with eight genes (yrbE4A, yrbE4B, mce4A, mce4B, mce4C, mce4D, mce4E and mce4F) of Mycobacterium tuberculosis. It expresses in the later phase of infection and imports cholesterol for long term survival of the bacilli. To cause latent infection, M. tuberculosis undergoes metabolic reprogramming of its genes to survive in the hostile environment like low availability of oxygen and nutrition depletion inside the host.. To analyze real time expression profile of mce4 operon under various stress conditions.. M. tuberculosis H37Rv was exposed to surface stress (0.1% SDS for 30min and 90min in late log and stationary phase of culture), hypoxia (5, 10, 15 and 20days) and grown in the presence of either glycerol or cholesterol as sole source of carbon. The expression profile of genes of mce4 operon was analyzed by real time PCR.. Surface stress induced expression of mce4C and yrbE4B in late log phase on 30min and 90min exposure respectively. The SDS exposure for 30min induced mce4C, mce4D and mce4F in stationary phase. All eight genes were induced significantly on 10th and 15th days of hypoxia and in the presence of cholesterol.. Hypoxia and cholesterol are potent factors for the expression of mce4 operon of M. tuberculosis.

Topics: Bacterial Proteins; Cholesterol; Detergents; Gene Expression Profiling; Glycerol; Humans; Hypoxia; Mycobacterium tuberculosis; Operon; Real-Time Polymerase Chain Reaction; Sodium Dodecyl Sulfate; Stress, Physiological

Pulmonary hypertension in response to chronic hypoxia is invariably accompanied by remodeling of the pulmonary vessels but the mechanism by which hypoxia increases the replication of vascular cells is unknown. To investigate the hypothesis that hypoxia stimulates intracellular kinase cascades we measured the activity of "classic" mitogen-activated protein (MAP) kinase pathways and "stress- activated" MAP kinase pathways in bovine pulmonary artery fibroblasts subjected to hypoxia for up to 30 h. Hypoxia (1% O2) stimulated strongly the stress-activated protein kinases, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase. Two peaks of p38 MAP kinase activity at 6 and 24 h were associated with an increase in the activity of mitogen-activated protein kinase-activated protein (MAPKAP) kinase-2, the immediate downstream target of p38 MAP kinase. Furthermore, the second phase of p38 MAP kinase activity could be reversed if cells were reoxygenated after 12 h. These data suggest that hypoxic stimulation of pulmonary artery cells is mediated by activation of the stress-activated protein kinases.

Topics: Animals; Blotting, Western; Calcium-Calmodulin-Dependent Protein Kinases; Cattle; Cell Division; Cells, Cultured; Chromatography, Ion Exchange; Chronic Disease; Electrophoresis, Polyacrylamide Gel; Fibroblasts; G1 Phase; Hypertension, Pulmonary; Hypoxia; Immunoblotting; Intracellular Signaling Peptides and Proteins; JNK Mitogen-Activated Protein Kinases; Mitogen-Activated Protein Kinases; Oxygen; p38 Mitogen-Activated Protein Kinases; Protein Serine-Threonine Kinases; Pulmonary Artery; S Phase; Sodium Dodecyl Sulfate; Time Factors

Topics: Animals; Brain; Brain Chemistry; Deoxycholic Acid; Depression, Chemical; Fatty Acids; Hypoxia; Oleic Acids; Phosphofructokinase-1; Rats; Sodium Dodecyl Sulfate