ArticleJournal of inflammation (London, England)2016
AG490 suppresses EPO-mediated activation of JAK2-STAT but enhances blood flow recovery in rats with critical limb ischemia.
Article in Journal of inflammation (London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- The novel GATA1-interacting protein HES6 is an essential transcriptional cofactor for human erythropoiesis.Nucleic acids research · 2023Article
- STAT5 as a Key Protein of Erythropoietin Signalization.International journal of molecular sciences · 2021Review
- The inhibition of miR‑101a‑3p alleviates H/R injury in H9C2 cells by regulating the JAK2/STAT3 pathway.Molecular medicine reports · 2020Article
- Neuroprotective Effects of AG490 in Neonatal Hypoxic-Ischemic Brain Injury.Molecular neurobiology · 2019Article
- Study on the mechanism of JAK2/STAT3 signaling pathway-mediated inflammatory reaction after cerebral ischemia.Molecular medicine reports · 2018Article
- "Do We Know Jack" About JAK? A Closer Look at JAK/STAT Signaling Pathway.Frontiers in oncology · 2018Review
- Microvascular anomaly conditions in psychiatric disease. Schizophrenia - angiogenesis connection.Neuroscience and biobehavioral reviews · 2017Review
- Inhibition of cerebral ischemia/reperfusion injury-induced apoptosis: nicotiflorin and JAK2/STAT3 pathway.Neural regeneration research · 2017Article
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5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundErythropoietin (EPO) has been demonstrated to enhance recovery in ischemic organs through enhancing angiogenesis. In this study, we used an experimental critical limb ischemia (CLI) rat model to reveal the underlying mechanisms and directly examine the benefits of the anti-apoptotic capacity of EPO in the acute phase of limb ischemia and following blood flow recovery.
methodsTo determine the role of the JAK2/STAT pathway in EPO-enhanced recovery after CLI, male Sprague-Dawley rats (n = 8 for each group) were divided into group 1 (normal control), group 2 (CLI treated with normal saline), group 3 (CLI treated with EPO), group 4 (CLI treated with AG490, a JAK2 inhibitor), and group 5 (CLI treated with EPO and AG490). Animals were sacrificed either at day 1 or day 14 and biochemical and histopathological examination of ischemic quadriceps were conducted.
resultsAt day 1, EPO administration reduced expression levels of apoptotic indices and activated the JAK2/STAT pathway; this activation was inhibited by additional AG490 treatment. Furthermore, the decrease in the size of the infarcted area, as well as activation of ERK1/2 and JNK showed similar regulatory trends with EPO or AG490 treatment. Of Interest, EPO and AG490 in combination showed a synergistic effect, increasing expression levels of antioxidants (GR, GPx, NQO-1) and decreasing transcriptional levels of pro-inflammatory factors (TNF-α, NF-kB). At day 14, laser Doppler analysis showed that the blood flow recovery was enhanced by EPO, AG490, or combined treatment.
conclusionAlthough inhibition of the JAK2/STAT pathways reduces the anti-apoptotic effects of EPO in the early phase of CLI, the benefits of AG490 in anti-inflammation and anti-oxidation still play a positive role in enhancing blood flow recovery after CLI.
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