Olympus master software version 1.42 download

miR-187-3p agomir further activated the ERS pathway and promoted apoptosis but decreased seipin expression levels these effects were reversed by miR-187-3p antagomir. I/R-induced ERS was closely associated with an increase in miR-1873p and a decrease in seipin expression. MCAO/R-induced morphological changes were analyzed with Nissl staining and Hematoxylin-eosin staining. TUNEL staining was used to assay apoptosis. Expression levels of miR-187-3p and proteins related to ERS and apoptosis were measured using RT-PCR, western blotting, immunofluorescence, and immunohistochemistry, respectively. PC12 cells were exposed to oxygenвЂ‘glucose deprivation/reoxygenation (OGD/R) to model I/R. Neurological deficits and infarction area were examined. A rat MCAO/R model was established by 1вЂЇh of occlusion and 24вЂЇh reperfusion. Therefore, we explored the involvement of miR-187-3p in I/R-induced ERS via the regulation of seipin. We previously reported that seipin is the target gene of miRвЂ‘187вЂ‘3p. Seipin is an endoplasmic reticulum protein that has recently been associated with ERS. miRNAs act as suppressors of gene expression and negatively regulate gene expression by targeting the protein-coding sequence (CDS) of specific target mRNAs.

Multiple microRNAs (miRNAs/miRs) are dysregulated during I/R and contribute to I/R-induced injury.

Ischemia/reperfusion (I/R) injury induces activation of the endoplasmic reticulum stress (ERS) pathway, accompanied by an increase in apoptosis.

Olympus master software version 1.42 download