[Effect of hypoxia on the expression of macrophage migration inhibitory factor (MIF) in rat vascular smooth muscle cells].

OBJECTIVE: To investigate whether hypoxia could induce the expression of MIF in vascular smooth muscle cells (VSMCs). METHODS: Rat vascular smooth muscle cells (A7r5 from ATCC) were cultured under hypoxia condition (37 degrees C, 5% CO2, 1% O2) and normoxia condition (37 degrees C, 5% CO2, 20% O2) for 2, 4, 12, 24 or 48 hours respectively. MIF mRNA expression was detected by reverse transcriptase and polymerase chain reaction (RT-PCR). MIF protein expression was determined by Enzyme-Linked Immunosorbent Assay (ELISA). RESULTS: Expression of MIF mRNA was up-regulated as early as 2 hours in VSMCs after being exposed to hypoxia condition, which remained the elevated level up to 48 hours. Meanwhile, MIF protein level increased after hypoxia treatment for 2 hours, and maintained elevated status up to 48 hours. CONCLUSION: Hypoxia could significantly induce MIF expression in VSMCs. MIF might be an important factor in the patho-physiological response of VSMCs to hypoxia.

[Study on the expression of activin-A in myocardial ischemia postconditioning].

OBJECTIVE: To analyze the relationship between the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) and to study the potential role of activin-A in myocardial ischemia postconditioning for the protection of myocardium. METHODS: Forty healthy adult Sprague-Dawley rats (gender unconcerned) were randomly divided into four different groups (n = 10 in each group): sham-operation, ischemia (I), ischemia/reperfusion (I/R) and ischemia postconditioning (postcon). In anesthetized open-chest rats, the left anterior descending artery (LAD) was ligated. Sham operation: the surgical procedure was identical to other groups, but the LAD was ligated for only 30 min, and not occluded. Ischemia: the LAD was occluded for 30 min; Ischemia/reperfusion: the LAD was occluded for 30 min and reperfused for 1 h; Postconditioning: after LAD occlusion for 30 min, at the start of reperfusion, three cycles of 30 s reperfusion and 30 s LAD re-occlusion preceded the 1h of reperfusion. The expression of activin-A in myocardium was detected by ELISA in all groups. The ability of suppression on the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) in myocardium taken from each group were measured by spectrophotometer. RESULTS: Compared with the sham-operated group, the expression of activin-A was significantly elevated in ischemia, ischemia/reperfusion and postconditiong groups, with the highest in the ischemia/reperfusion group. And postconditioning significantly decreased the expression of activin-A in the ischemia/ reperfusion injured myocardium [(343.05 +/- 25.8) microg/mg protein vs (470.6 +/- 33.1) microg/mg protein, P < 0.05]. The expression of activin-A was negatively correlated with the ability of suppression on the hydroxy free radical and LDH separately. CONCLUSION: The result indicated that activin-A was involved in myocardial ischemia/reperfusion injury, and down-regulation of activin-A might be one of the cardioprotective mechanisms of postconditioning.