lithium-chloride has been researched along with Asthma* in 2 studies
2 other study(ies) available for lithium-chloride and Asthma
| Article | Year |
|---|---|
Onset of abnormal movements and cardiovascular symptoms after acute change in complex polypharmacy in a child with attention-deficit/hyperactivity disorder and mood symptoms.
Topics: Adrenergic alpha-Agonists; Antimanic Agents; Antipsychotic Agents; Aripiprazole; Asthma; Attention Deficit Disorder with Hyperactivity; Cardiovascular Diseases; Chest Pain; Child; Dyskinesia, Drug-Induced; Family; Female; Guanfacine; Humans; Lithium Chloride; Male; Mood Disorders; Neuropsychological Tests; Obesity; Paroxetine; Piperazines; Polypharmacy; Pregnancy; Prenatal Exposure Delayed Effects; Psychomotor Agitation; Quinolones; Selective Serotonin Reuptake Inhibitors; Smoking; Social Environment | 2012 |
Inhibition of glycogen synthase kinase-3beta is sufficient for airway smooth muscle hypertrophy.
We examined the role of glycogen synthase kinase-3beta (GSK-3beta) inhibition in airway smooth muscle hypertrophy, a structural change found in patients with severe asthma. LiCl, SB216763, and specific small interfering RNA (siRNA) against GSK-3beta, each of which inhibit GSK-3beta activity or expression, increased human bronchial smooth muscle cell size, protein synthesis, and expression of the contractile proteins alpha-smooth muscle actin, myosin light chain kinase, smooth muscle myosin heavy chain, and SM22. Similar results were obtained following treatment of cells with cardiotrophin (CT)-1, a member of the interleukin-6 superfamily, and transforming growth factor (TGF)-beta, a proasthmatic cytokine. GSK-3beta inhibition increased mRNA expression of alpha-actin and transactivation of nuclear factors of activated T cells and serum response factor. siRNA against eukaryotic translation initiation factor 2Bepsilon (eIF2Bepsilon) attenuated LiCl- and SB216763-induced protein synthesis and expression of alpha-actin and SM22, indicating that eIF2B is required for GSK-3beta-mediated airway smooth muscle hypertrophy. eIF2Bepsilon siRNA also blocked CT-1- but not TGF-beta-induced protein synthesis. Infection of human bronchial smooth muscle cells with pMSCV GSK-3beta-A9, a retroviral vector encoding a constitutively active, nonphosphorylatable GSK-3beta, blocked protein synthesis and alpha-actin expression induced by LiCl, SB216763, and CT-1 but not TGF-beta. Finally, lungs from ovalbumin-sensitized and -challenged mice demonstrated increased alpha-actin and CT-1 mRNA expression, and airway myocytes isolated from ovalbumin-treated mice showed increased cell size and GSK-3beta phosphorylation. These data suggest that inhibition of the GSK-3beta/eIF2Bepsilon translational control pathway contributes to airway smooth muscle hypertrophy in vitro and in vivo. On the other hand, TGF-beta-induced hypertrophy does not depend on GSK-3beta/eIF2B signaling. Topics: Animals; Asthma; Bronchi; Cytokines; Enzyme Inhibitors; Eukaryotic Initiation Factor-2B; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Humans; Hypertrophy; Indoles; Lithium Chloride; Maleimides; Mice; Muscle Proteins; Muscle, Smooth; Protein Biosynthesis; RNA, Small Interfering; Signal Transduction | 2008 |