Erythropoietin Ameliorates Lung Injury by Accelerating Pulmonary Endothelium Cell Proliferation via Janus Kinase-Signal Transducer and Activator of Transcription 3 Pathway After Kidney Ischemia and Reperfusion Injury

Zhu, Minyan; Wang, L.; Yang, Jian; Xie, Keliang; Liu, S.; Xu, Chen; Wang, J.; Gu, Leyi; Ni, Zhaohui; Xu, Gaolian; Che, Miaolin

doi:10.1016/j.transproceed.2019.01.059

Cited by 23 publications

(13 citation statements)

References 22 publications

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“…Several reports exist demonstrating beneficial EPO effects on acute lung injury and the acute respiratory distress syndrome (ARDS) in various different animal models (reviewed in (Kakavas et al 2011)). EPO appears to exert its pleiotropic actions in the lung by protecting the integrity of the pulmonary epithelial and endothelial cells as well as by attenuating the associated pulmonary interstitial and alveolar epithelial edema and the deterioration of pulmonary oxygenation function (Kakavas et al 2011;Zhu et al 2019). This is achieved via modulating multiple levels of early signaling pathways involved in apoptosis, inflammation and peroxidation, potentially restoring overall homeostasis (Kakavas et al 2011;Anagnostou et al 1990;MacRedmond et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin as candidate for supportive treatment of severe COVID-19

Ehrenreich

Weißenborn

Begemann

et al. 2020

Mol Med

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In light of the present therapeutic situation in COVID-19, any measure to improve course and outcome of seriously affected individuals is of utmost importance. We recap here evidence that supports the use of human recombinant erythropoietin (EPO) for ameliorating course and outcome of seriously ill COVID-19 patients. This brief expert review grounds on available subject-relevant literature searched until May 14, 2020, including Medline, Google Scholar, and preprint servers. We delineate in brief sections, each introduced by a summary of respective COVID-19 references, how EPO may target a number of the gravest sequelae of these patients. EPO is expected to: (1) improve respiration at several levels including lung, brainstem, spinal cord and respiratory muscles; (2) counteract overshooting inflammation caused by cytokine storm/ inflammasome; (3) act neuroprotective and neuroregenerative in brain and peripheral nervous system. Based on this accumulating experimental and clinical evidence, we finally provide the research design for a double-blind placebo-controlled randomized clinical trial including severely affected patients, which is planned to start shortly.

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Section: Introductionmentioning

confidence: 99%

Erythropoietin as candidate for supportive treatment of severe COVID-19

Ehrenreich

Weißenborn

Begemann

et al. 2020

Mol Med

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“…This process may contribute to cardioprotection in ischemic injury, a condition characterized by the release of nuclear factor κB (NF-κB), reactive oxygen species (ROS) accumulation and inflammation. In this context, previous studies have shown that Epo increased endothelial cell proliferation and neovascularization (Doleschel et al 2015;Zhu et al 2019).…”

Section: Introductionmentioning

confidence: 93%

Role of protein tyrosine phosphatase 1B (PTP1B) in the increased sensitivity of endothelial cells to a promigratory effect of erythropoietin in an inflammatory environment

Chamorro

Maltaneri

Schiappacasse

et al. 2020

Biological Chemistry

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The proliferation and migration of endothelial cells are vascular events of inflammation, a process which can also potentiate the effects of promigratory factors. With the aim of investigating possible modifications in the activity of erythropoietin (Epo) in an inflammatory environment, we found that Epo at a non-promigratory concentration was capable of stimulating EA.hy926 endothelial cell migration when TNF-α was present. VCAM-1 and ICAM-1 expression, as well as adhesion of monocytic THP-1 cells to endothelial layers were also increased. Structurally modified Epo (carbamylation or N-homocysteinylation) did not exhibit these effects. The sensitizing effect of TNF-α on Epo activity was mediated by the Epo receptor. Inhibition assays targeting the PI3K/mTOR/NF-κB pathway, shared by Epo and TNF-α, show a crosstalk between both cytokines. As observed in assays using antioxidants, cell migration elicited by TNF-α+Epo depended on TNF-α-generated reactive oxygen species (ROS). ROS-mediated inactivation of protein tyrosine phosphatase 1B (PTP1B), involved in Epo signaling termination, could explain the synergistic effect of these cytokines. Our results suggest that ROS generated by inflammation inactivate PTP1B, causing the Epo signal to last longer. This mechanism, along with the cross-talk between both cytokines, could explain the sensitizing action of TNF-α on the migratory effect of Epo.

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“…(Fig. 1) (23,55). In addition, the cytokines interleukin (IL)-4 and IL-13 can activate the JAK3/STAT6 signaling pathway (Fig.…”

Section: Signal Transduction Of Macrophages In Akimentioning

confidence: 99%

Major signaling pathways and key mediators of macrophages in acute kidney injury (Review)

Chen

Wang³

et al. 2021

Mol Med Rep

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Acute kidney injury (AKI) has become a global public health problem with high morbidity and mortality rates, as well as high healthcare costs. Immune cells, particularly macrophages, which regulate tissue development, destroy pathogens, control homeostasis and repair wounds, play crucial and complex roles in AKI. In various types of AKI, numerous rapidly recruited monocytes and tissue-resident macrophages act in a coordinated manner. Thus, elucidating the phenotypic and functional characteristics of macrophages in AKI is essential for identifying potential therapeutic targets. Macrophage-sensing mediators and macrophage-derived mediators participate in the major macrophage-related signaling pathways in AKI, which regulate macrophage polarization and determine disease progression. In conclusion, macrophages change their roles and regulatory mechanisms during the occurrence and development of AKI. The aim of the present review was to contribute to an improved understanding of AKI and to the identification of novel therapeutic targets for this condition.

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Erythropoietin Ameliorates Lung Injury by Accelerating Pulmonary Endothelium Cell Proliferation via Janus Kinase-Signal Transducer and Activator of Transcription 3 Pathway After Kidney Ischemia and Reperfusion Injury

Cited by 23 publications

References 22 publications

Erythropoietin as candidate for supportive treatment of severe COVID-19

Erythropoietin as candidate for supportive treatment of severe COVID-19

Role of protein tyrosine phosphatase 1B (PTP1B) in the increased sensitivity of endothelial cells to a promigratory effect of erythropoietin in an inflammatory environment

Major signaling pathways and key mediators of macrophages in acute kidney injury (Review)

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