Abstract
Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia (ACI), we established a middle cerebral artery occlusion (MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor β (GMFB) based on quantitative analysis of the global rat serum proteome. Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was over-expressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation (OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium (CM) after OGD. We then used the CM to culture pulmonary microvascular endothelial cells (PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover, ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells. In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.
Highlights
Acute cerebral ischemia (ACI) is a recognized disease that can severely damage health, and has high mortality and morbidity [1,2,3,4]
We showed that glia maturation factor beta (GMFB) derived from astrocytes directly damaged pulmonary microvascular endothelial cells (PMVECs)
Since acute cerebral ischemia (ACI) led to pulmonary edema and lung inflammation, we aimed to determine whether certain factors that were abnormally expressed due to the damage to the brain permeated into the blood and caused injury to PMVECs in lung tissue
Summary
Acute cerebral ischemia (ACI) is a recognized disease that can severely damage health, and has high mortality and morbidity [1,2,3,4]. Clinical data indicate that patients with brain damage are often diagnosed with dysfunction and even failure of other organs [15,16,17,18,19,20]. Lung injury induced by stroke is termed neurogenic pulmonary edema, which is often characterized by aseptic inflammation of the lungs and pulmonary edema [22]. Few researchers have concentrated on the molecular mechanisms of neurogenic pulmonary edema, and the existing research has not fully elucidated the pathological processes underlying this condition
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