Journal: Inflammopharmacology
Article Title: Cyclooxygenase-2 activates EGFR–ERK1/2 pathway via PGE2-mediated ADAM-17 signaling in testosterone-induced benign prostatic hyperplasia
doi: 10.1007/s10787-022-01123-7
Figure Lengend Snippet: Graphical diagram of functional correlation between inflammation and hyperplasia in TST-induced BPH. Cycloxygenase-2 (COX-2) upregulates EGFR–ERK1/2 signaling cascade via stimulation of PGE2-induced ADAM-17 and consequent shedding of TGF-α: The left panel (in red color ) shows that TST-induced BPH stimulates the nuclear translocation of NF-κB [ 1–2 ] resulting in increasing gene transcription of COX-2 [ 3 ] and subsequent PGE2 [ 4 ]. PGE2 trans-activates EGFR via intracellular activation of ADAM-17 (TACE) [ 5 ] leading to shedding of TGF-α [ 6 ]. Consequently, active TGF-α phosphorylates EGFR and induce ERK1/2 phosphorylation [ 7–8 ]. Together, the nuclear translocation of p-ERK1/2 [ 9 ] induced prostatic hyperplasia via enhancing gene expression of cyclin D1 and anti-apoptotic Bcl-2 in consistent with downregulation of pro-apoptotic Bax expression. In the contrast, the panel in the right corner (in blue color ) shows the potential effect of COX-2 inhibition in TST-induced BPH
Article Snippet: In accordance with the manufacturer’s protocol, the assessment of COX-2 (Cusabio ® , Houston, USA), NF-κB (Elabscience ® , Houston, USA), PGE2 (Elabscience ® , Houston, USA), IL-6 (Immuno-Biological Laboratories ® , Minneapolis, USA), TNF-α (Cloud-Clone Corp. ® , Texas, USA), ADAM-17 or TACE (Elabscience ® , Houston, USA), and TGF-α (LifeSpan Biosciences ® , Houston, USA) in prostatic tissue homogenates was performed using the corresponding rat ELISA kits.
Techniques: Functional Assay, Translocation Assay, Activation Assay, Phospho-proteomics, Gene Expression, Expressing, Inhibition
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![Graphical diagram of functional correlation between inflammation and hyperplasia in TST-induced BPH. Cycloxygenase-2 (COX-2) upregulates EGFR–ERK1/2 signaling cascade via stimulation of PGE2-induced ADAM-17 and consequent shedding of TGF-α: The left panel (in red color ) shows that TST-induced BPH stimulates the nuclear translocation of NF-κB [ 1–2 ] resulting in increasing gene transcription of COX-2 [ 3 ] and subsequent PGE2 [ 4 ]. PGE2 trans-activates EGFR via intracellular activation of ADAM-17 (TACE) [ 5 ] leading to shedding of TGF-α [ 6 ]. Consequently, active TGF-α phosphorylates EGFR and induce ERK1/2 phosphorylation [ 7–8 ]. Together, the nuclear translocation of p-ERK1/2 [ 9 ] induced prostatic hyperplasia via enhancing gene expression of cyclin D1 and anti-apoptotic Bcl-2 in consistent with downregulation of pro-apoptotic Bax expression. In the contrast, the panel in the right corner (in blue color ) shows the potential effect of COX-2 inhibition in TST-induced BPH](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_8186/pmc09958186/pmc09958186__10787_2022_1123_Fig8_HTML.jpg)