We found that FIZZ1/RELM.alpha. is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM.alpha. was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM.alpha. protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

The John Hopkins University

Method of treating hypertrophic cardiomyopathy

Two novel phosphorylation sites of myosin light chain 1 (MLC1) are described. Methods of monitoring phosphorylation of MLC1 to identify new cardiac and skeletal muscle protective agents, monitor the extent of preconditioning of cardiac and skeletal muscles, and monitoring the status of a subject with cardiac or skeletal muscle damage are provided. Also provided are methods and compositions for altering MLC1 to change contractility of cardiac and skeletal muscles and to protecting cardiac and skeletal muscles from damage caused by conditions and/or agents including, but not limited to, cardiomyopathies, hypertension, free radicals ischemia, hypoxia, and ischemia/hypoxia with reperfusion.

Queens University at Kingston

Methods and compositions relating to phosphorylated myosin light chain 1

A method of combatting, e.g., preventing as well as treating, a disease state such as cystic fibrosis, neonatal hypoxemia, pulmonary hypertension, adult respiratory distress syndrome, psoriasis, spondyloarthritis, rheumatoid arthritis, gout, inflammatory bowel disease, myocardial infarctions, and/or osteoporosis in an animal subject, by administering to the animal subject an amount of an organic boron compound which is effective thereagainst. The organic boron compounds usefully employed in the method of the invention include any suitable organic boron-containing compounds, such as Lewis base-boron adducts; a preferred class of organic boron compounds useful in such method includes boron analogs of .alpha.-amino acids, and the corresponding amides and esters of such amino acids. A method is also disclosed of inhibiting enzyme activity in in vitro or in vivo systems comprising administering to such system an enzyme-inhibiting amount of an organic boron compound. Further disclosed is a method of reducing hydroxyproline, calcium, and/or inorganic phosphorous in serum and/or urine of an animal subject, by administering to the animal subject an effective amount of an organic boron compound.

cardiomyopathies/hypoxia

Method of treating hypertrophic cardiomyopathy

Methods and compositions relating to phosphorylated myosin light chain 1

Method of combatting osteoporosis in mammalian subjects, utilizing organic boron compounds

Database tanaman obat terlengkap yang didukung oleh sains