MiR-21 participates in the neuroprotection of diazoxide against hypoxic-ischemia encephalopathy by targeting PDCD4

Chen, Yuxia; Zeng, Hao; Liu, Huayan

doi:10.1080/02699052.2022.2087906

Cited by 3 publications

(1 citation statement)

References 35 publications

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“…In a newborn piglet model, diazoxide protects postischemic vascular reactivity to carbon dioxide, an indicator of endothelial function in ischemia-reperfusion injury, contributing to neuroprotection [50]. Additionally, diazoxide preserves neuronal function by enhanced cellular protection after ischemia/reperfusion by activation of mitochondrial K ATP channels and preconditioning of cerebral endothelium and a protects the blood-brain barrier from ischemic stress [51,52], potentially via the PI3K/AKT pathway [53].…”

Section: Current Evidence On Diazoxide Use In Neonatesmentioning

confidence: 99%

Diazoxide for Neonatal Hyperinsulinemic Hypoglycemia and Pulmonary Hypertension

2022

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Hypoglycemia in neonates is associated with long-term neurodevelopmental effects. Hyperinsulinemic hypoglycemia (HH) is the most common cause of persistent hypoglycemia in neonatal intensive care units. Diazoxide is the only medication that is currently recommended for treatment of HH in neonates. However, the use of diazoxide in neonates is associated with pulmonary hypertension as an adverse effect. In this article, we review the literature on the mechanism of action and adverse effects with the use of diazoxide in neonatal hyperinsulinism. We then present a case series of neonates treated with diazoxide in our neonatal intensive care unit over a 5-year period. Among 23 neonates who received diazoxide, 4 developed pulmonary hypertension and 1 died. All infants who developed pulmonary hypertension were born preterm at less than 36 weeks gestation and had pre-existing risk factors for pulmonary hypertension. HH in preterm neonates, with pre-existing pulmonary hypertension or with risk factors for pulmonary hypertension requires thoughtful management.

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Section: Current Evidence On Diazoxide Use In Neonatesmentioning

confidence: 99%

Diazoxide for Neonatal Hyperinsulinemic Hypoglycemia and Pulmonary Hypertension

2022

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Correlation Study on the Prognostic Value of miR-21 and S-100B Protein Levels in Neonatal Hypoxic-Ischemic Encephalopathy Undergoing Hypothermia Therapy

Liu,

Liu

2024

International Journal of Neuroscience

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Knockdown of IGF2BP3 Down-Regulates PDCD4 Levels to Attenuate Hypoxic-Ischemic Brain Damage

Chen,

Fang,

Liu

et al. 2024

Front. Biosci. (Landmark Ed)

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Background: Hypoxic-ischemic brain damage (HIBD) is a prevalent brain injury with high mortality and morbidity. It results from hypoxia and ischemia of the brain due to various perinatal factors. A previous study showed that knockdown of programmed cell death factor 4 (PDCD4) could reduce infarction injury resulting from ischemia/reperfusion injury. However, exact mechanism by which PDCD4 acts in HIBD is not yet understood. Our aim in present investigation was to investigate the function and mechanism of PDCD4 in alleviating HIBD. Methods: An HIBD model was developed using neonatal rats. After 48 h of modeling, short-term neurological function was evaluated and the brain tissue removed for assessment of cerebral infarct volume and brain water content (BWC). A cell model of oxygen glucose deprivation/reoxygenation (OGD/R) was also constructed. Overexpression or knockdown of insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) or PDCD4 was performed in pretreated cells. Results: The geotaxis reflex time, cerebral infarct volume, and BWC all increased after HIBD in this neonatal rat model. Additionally, the levels of PDCD4 and of the N6-Methyladenosine (m6A) reader protein IGF2BP3 were increased in HIBD rats and OGD/R-stimulated pheochromocytoma (PC12) cells relative to controls. Moreover, OGD/R-stimulated pheochromocytoma PC12 cells showed decreased cell viability, increased apoptosis, and elevated Interleukin 6 (IL-6), Interleukin 1 β (IL-1β), and tumor necrosis factor-α (TNF-α) contents. These features were reversed after knocking down IGF2BP3. The interaction between IGF2BP3 protein and PDCD4 mRNA was confirmed by RNA immunoprecipitation and RNA pull-down assays. Furthermore, knockdown of IGF2BP3 in OGD/R-stimulated PC12 cells reduced cell damage via down-regulation of PDCD4. Finally, the IGF2BP3/PDCD4 axis alleviated OGD/R-induced cell injury in primary cortical neurons (PCNs). Conclusions: PDCD4 and m6A reader protein IGF2BP3 were up-regulated in an HIBD neonatal rat model. Knockdown of IGF2BP3 in OGD/R-stimulated PC12 cells or PCNs alleviated cell damage through reducing PDCD4.

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MiR-21 participates in the neuroprotection of diazoxide against hypoxic-ischemia encephalopathy by targeting PDCD4

Cited by 3 publications

References 35 publications

Diazoxide for Neonatal Hyperinsulinemic Hypoglycemia and Pulmonary Hypertension

Diazoxide for Neonatal Hyperinsulinemic Hypoglycemia and Pulmonary Hypertension

Correlation Study on the Prognostic Value of miR-21 and S-100B Protein Levels in Neonatal Hypoxic-Ischemic Encephalopathy Undergoing Hypothermia Therapy

Knockdown of IGF2BP3 Down-Regulates PDCD4 Levels to Attenuate Hypoxic-Ischemic Brain Damage

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