Carbamylated erythropoietin enhances mice ventilatory responses to changes in O2 but not CO2 levels

Khemiri, Hanan; Maresca, Marc; Gestreau, Christian

doi:10.1016/j.resp.2016.06.002

Cited by 3 publications

(3 citation statements)

References 60 publications

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“…With the development of studying, recently, CEPO has been extended to other areas about the protective effects in addition to nervous system, kidney and heart as discussed above. In these studies, CEPO was supposed to be highly effective of wound healing (37), improving breathing during hypoxia (38), and attenuating cognitive effects of electroconvulsive therapy (39).…”

Section: Cepo-mediated Protection In Other Organs and Tissuesmentioning

confidence: 99%

Carbamylated Erythropoietin and Its Role of Tissue Protection

Li¹,

Diao²,

Ma³

et al. 2017

J Anesth Perioper Med

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Aim of review:We reviewed the study of carbamylated erythropoietin (CEPO) and its probable mechanism involved in the regulation of tissue-protection. Methods: Recent published literatures in this area were inclusive and reviewed. Recent findings: CEPO has equivalent tissue-protective properties as recombinant human erythropoietin (rhEPO) but with non-erythropoietic effects. It shows protective properties on nervous system, heart, kidney and some other organs, which are associated with inhibition of apoptosis, restoration of vascular autoregulation and attenuation of inflammatory responses. However, the underlying mechanism of CEPO responsible for its beneficial effects is still not well-known. Summary: CEPO gradually turned into a promising drug candidate at least for many diseases caused by ischemia reperfusion injury. The safety and efficacy of CEPO in clinical are warranted in the future.

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Section: Cepo-mediated Protection In Other Organs and Tissuesmentioning

confidence: 99%

Carbamylated Erythropoietin and Its Role of Tissue Protection

Li¹,

Diao²,

Ma³

et al. 2017

J Anesth Perioper Med

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“…; Khemiri et al. ). Moreover, testing at these time points ensured that results were not compounded by handling procedures that are inherent to i.p.…”

Section: Introductionmentioning

confidence: 96%

Saline as a vehicle control does not alter ventilation in male CD-1 mice

2018

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Saline (0.9% NaCl) is used in clinical and research settings as a vehicle for intravenous drug administration. While saline is a standard control in mouse studies, there are reports of hyperchloremic metabolic acidosis in high doses. It remains unknown if metabolic acidosis occurs in mice and/or if compensatory increases in breathing frequency and tidal volume accompany saline administration. It was hypothesized that saline administration alters blood pH and the pattern of breathing in conscious CD‐1 male mice exposed to air or hypoxia (10% O2, balanced N2). Unrestrained barometric plethysmography was used to quantify breathing frequency (breaths/min; bpm), tidal volume (VT; mL/breath/10 g body weight (BW)), and minute ventilation (VE; mL/min/10 g BW) in two designs: (1) 11‐week‐old mice with no saline exposure (n = 11) compared to mice with 7 days of 0.9% saline administration (intraperitoneal, i.p.; 10 mL/kg body mass; n = 6). and (2) 17‐week‐old mice tested before (PRE) and after 1 day (POST1, n = 6) or 7 days (POST7, n = 5) of saline (i.p.; 10 mL/kg body mass). There were no differences when comparing frequency, VT, or VE between groups for either design with room air or hypoxia exposures. Hypoxia increased frequency, VT, and VE compared to room air. Moreover, conscious blood sampling showed no differences in pH, pa CO 2, paO2, or HCO3− in mice without or with 7 days of saline. These findings reveal no differences in ventilation following 1 and/or 7 days of saline administration in mice. Therefore, the use of 0.9% saline as a control is supported for studies evaluating the control of breathing in mice.

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“…Indeed, absence or drastic reduction of the CO 2 /H + sensitivity leads to central hypoventilation syndromes such as Ondine’s curse ( Weese-Mayer et al, 2010 ; Ramanantsoa et al, 2011 ). Conclusions of the few studies conducted on this topic do not reach consensus ( Ballot et al, 2015b ; Khemiri et al, 2016 ; Laouafa et al, 2016 , 2017 ; Menuet et al, 2016 ; Silva et al, 2017 ). Menuet and collaborators reported a decrease in HcVR in adult transgenic mice over-expressing brain Epo, suggesting that an excess of Epo limits the CO 2 /H + respiratory response ( Menuet et al, 2016 ).…”

Section: Introductionmentioning

confidence: 98%

In Transgenic Erythropoietin Deficient Mice, an Increase in Respiratory Response to Hypercapnia Parallels Abnormal Distribution of CO2/H+-Activated Cells in the Medulla Oblongata

et al. 2022

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Erythropoietin (Epo) and its receptor are expressed in central respiratory areas. We hypothesized that chronic Epo deficiency alters functioning of central respiratory areas and thus the respiratory adaptation to hypercapnia. The hypercapnic ventilatory response (HcVR) was evaluated by whole body plethysmography in wild type (WT) and Epo deficient (Epo-TAgh) adult male mice under 4%CO2. Epo-TAgh mice showed a larger HcVR than WT mice because of an increase in both respiratory frequency and tidal volume, whereas WT mice only increased their tidal volume. A functional histological approach revealed changes in CO2/H+-activated cells between Epo-TAgh and WT mice. First, Epo-TAgh mice showed a smaller increase under hypercapnia in c-FOS-positive number of cells in the retrotrapezoid nucleus/parafacial respiratory group than WT, and this, independently of changes in the number of PHOX2B-expressing cells. Second, we did not observe in Epo-TAgh mice the hypercapnic increase in c-FOS-positive number of cells in the nucleus of the solitary tract present in WT mice. Finally, whereas hypercapnia did not induce an increase in the c-FOS-positive number of cells in medullary raphe nuclei in WT mice, chronic Epo deficiency leads to raphe pallidus and magnus nuclei activation by hyperacpnia, with a significant part of c-FOS positive cells displaying an immunoreactivity for serotonin in the raphe pallidus nucleus. All of these results suggest that chronic Epo-deficiency affects both the pattern of ventilatory response to hypercapnia and associated medullary respiratory network at adult stage with an increase in the sensitivity of 5-HT and non-5-HT neurons of the raphe medullary nuclei leading to stimulation of fR for moderate level of CO2.

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Carbamylated erythropoietin enhances mice ventilatory responses to changes in O2 but not CO2 levels

Cited by 3 publications

References 60 publications

Carbamylated Erythropoietin and Its Role of Tissue Protection

Carbamylated Erythropoietin and Its Role of Tissue Protection

Saline as a vehicle control does not alter ventilation in male CD-1 mice

In Transgenic Erythropoietin Deficient Mice, an Increase in Respiratory Response to Hypercapnia Parallels Abnormal Distribution of CO2/H+-Activated Cells in the Medulla Oblongata

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