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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Actins, Animals, Calcium-Binding Proteins, Cell Hypoxia, Cell Proliferation, Cells, Cultured, Glycoproteins, Microfilament Proteins, Myocytes, Smooth Muscle, PPAR gamma, Phenotype, Pulmonary Artery, Rats, Rats, Sprague-Dawley, Up-Regulation.
user
Does [ Ulinastatin inhibit hypoxia-induced phenotype modulation of pulmonary artery smooth muscle cells by up-regulating PPAR-γ expression ]? Context: To evaluate the effect of ulinastatin on hypoxia-induced phenotype modulation of pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. Cultured PASMCs from SD rats were exposed to normoxic condition, normoxia with ulinastatin treatment, hypoxia, or hypoxia with ulinastatin treatment. After 24 h of exposures, the cells were examined for SM-α-actin and caplonin expressions with immunofluorescence assay and for cell migration with CCK-8 and  Ulinastatin obviously enhanced the expressions of SM-α-actin and calponin (P<0.05), inhibited the proliferation and migration (P<0.05), and up-regulated the expression of PPAR-γ in PASMCs exposed to hypoxia (P<0.05). Pretreatment of the cells with GW9662 abolished the effect of ulinastatin on hypoxia-induced phenotype modulation of PASMCs and enhanced the cell proliferation and migration (P<0.05).
assistant
Ulinastatin inhibits hypoxia-induced phenotype modulation of PASMCs from rats possibly by up-regulating the expression of PPAR-γ. Final Decision: yes