کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1929599 | 1050469 | 2012 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: The new role of LOX-1 in hypertension induced neuronal apoptosis The new role of LOX-1 in hypertension induced neuronal apoptosis](/preview/png/1929599.png)
Lectin-like oxidized low-density lipoprotein (oxLDL) receptor-1 (LOX-1) was originally identified as a receptor for oxLDL predominantly expressed in endothelial cells. Recently up-regulation of LOX-1 has been implicated in oxidative stress and cell apoptosis in many cell types. However, LOX-1 expression in neurons or regulation of neuronal apoptosis by LOX-1 has not been reported. To investigate the possible roles of LOX-1 in hypertension induced brain damage, we examined the distribution of LOX-1 in cortex and hippocampus and compared its expression in 32-week-old SHR and WKY rats. Immunofluorescence revealed that LOX-1 positive cells were located principally at the cortex involved in sensory information processing and were mainly expressed in neurons. We also found up-regulated mRNA expression of LOX-1, Bax and caspase-3 and down-regulated mRNA expression of Bcl-2 in SHR group. Compared with WKY group, SHR group showed increased LOX-1 positive cells and TUNEL positive cells. Furthermore, double-labeling method indicated that LOX-1 expression was colocalized with TUNEL positive cells, which means that LOX-1 expression was involved in hypertension related cell apoptosis. These findings indicated that LOX-1 expression was up-regulated in the cortex of SHR and its expression has implication in neuronal apoptosis. Elevated Bax/Bcl-2 ratio may be involved under this event.
• LOX-1 was expressed in neurons of cortex involved in sensory information processing.
• SHR group showed more LOX-1-positive neurons compared with age-matched WKY rats.
• LOX-1 was colocalized with apoptotic cells and was involved in neuronal apoptosis.
• Elevated Bax/Bcl-2 expression ratio may be under LOX-1 related neuronal apoptosis.
Journal: Biochemical and Biophysical Research Communications - Volume 425, Issue 4, 7 September 2012, Pages 735–740