miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

Wu, Jizhi; Zhang, Guangqi; Xiong, Hui; Zhang, Yuguang; Ding, Gang; Ge, Junfeng

doi:10.1038/s41598-021-95712-1

Cited by 6 publications

(3 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…22,23 In addition, miR-181c-5p not only mediates the apoptosis of vascular endothelial cells induced by hyperoxemia but also enhances the inflammatory response following an ischemic stroke. 24,25 Our study discovered that miR-181c-5p's down-regulation might prevent hypoxic PMVECs from going into apoptosis by controlling the amounts of proteins involved in the apoptotic signalling pathway, the release of inflammatory mediators, and the level of vasoactive molecules.…”

Section: Discussionmentioning

confidence: 92%

Long noncoding RNA ANRIL alleviates hypoxia‐induced pulmonary microvascular endothelial cell damage

Qi,

Chen,

Zhang

et al. 2024

Eur J Clin Investigation

View full text Add to dashboard Cite

BackgroundHigh‐altitude pulmonary oedema (HAPE) is a form of noncardiogenic pulmonary oedema. Studies have found that long noncoding RNA (lncRNA) plays an important role in HAPE. ANRIL is significant in pulmonary illnesses, which implies that alterations in ANRIL expression levels may be involved in the beginning and development of HAPE. However, the specific mechanism is indistinct. The present study is meant to explore the effect and mechanism of ANRIL on hypoxic‐induced injury of pulmonary microvascular endothelial cells (PMEVCs).MethodsIn the hypoxic model of PMVECs, overexpression of ANRIL or knockdown of miR‐181c‐5p was performed to assess cell proliferation, apoptosis, and migration. Furthermore, the levels of apoptosis‐related proteins, inflammatory factors, and vascular active factors were also measured.ResultsThe results showed that, after 24 h of hypoxia, PMVECs proliferation and migration were suppressed in comparison to the control group, along with an increase in apoptosis, a decrease in the expression of ANRIL, and an increase in the expression of miR‐181c‐5p (all p < .05). The damage caused by hypoxia in PMVECs can be lessened by overexpressing ANRIL, which also inhibits the production of TNF‐α, iNOS, and VEGF as well as BAX and cleaved caspase‐3 (all p < .05). Further experimental results showed that overexpression of ANRIL and knockdown of miR‐181c‐5p had the same protection against hypoxic injury in PMVECs (all p < .05).ConclusionsOur study suggests that ANRIL may prevent hypoxia injury to PMVECs in HAPE through the negative regulation of miR‐181c‐5p.

show abstract

Section: Discussionmentioning

confidence: 92%

Long noncoding RNA ANRIL alleviates hypoxia‐induced pulmonary microvascular endothelial cell damage

Qi,

Chen,

Zhang

et al. 2024

Eur J Clin Investigation

View full text Add to dashboard Cite

show abstract

“…Concurrently, the inflammatory milieu might disrupt normal glucose metabolism, amplifying susceptibility to cardiovascular events and mortality ( 36 , 37 ). In addition, high oxygen saturation might induce cellular damage, encompassing apoptosis and necrosis, exacerbating brain tissue injury and worsening cerebral infarction ( 38 , 39 ).…”

Section: Discussionmentioning

confidence: 99%

Association between SpO2 and the risk of death in elderly T2DM patients with cerebral infarction: a retrospective cohort study

Zhang,

Ji,

Gao

et al. 2024

Front. Neurol.

View full text Add to dashboard Cite

ObjectiveThis study aimed to evaluate the SpO2 (transcutaneous oxygen saturation) -mortality link in elderly T2DM (diabetes mellitus type 2) patients with cerebral infarction and identify their optimal SpO2 range.MethodsIn this investigation, we employed a comprehensive approach. Initially, we screened the MIMIC-IV database, identifying elderly T2DM patients with cerebral infarction, utilizing specific ICD-9 and ICD-10 codes. We then harnessed the power of restricted cubic splines to craft a visual representation of the correlation between SpO2 and 1-year mortality. To enhance our analysis, we harnessed Cox multivariate regression, allowing us to compute adjusted hazard ratios (HR) accompanied by 95% confidence intervals (CIs). Additionally, we crafted Cumulative Mortality Curve analyses, augmenting our study by engaging in rigorous subgroup analyses, stratifying our observations based on pertinent covariates.ResultsIn this study, 448 elderly T2DM patients with cerebral infarction were included. Within 1-year post-discharge, 161 patients (35.94%) succumbed. Employing Restricted Cubic Spline analysis, a statistically significant U-shaped non-linear relationship between admission ICU SpO2 levels and 1-year mortality was observed (P-value < 0.05). Further analysis indicated that both low and high SpO2 levels increased the mortality risk. Cox multivariate regression analysis, adjusting for potential confounding factors, confirmed the association of low (≤94.5%) and high SpO2 levels (96.5–98.5%) with elevated 1-year mortality risk, particularly notably high SpO2 levels (>98.5%) [HR = 2.06, 95% CI: 1.29–3.29, P-value = 0.002]. The cumulative mortality curves revealed the following SpO2 subgroups from high to low cumulative mortality at the 365th day: normal levels (94.5% < SpO2 ≤ 96.5%), low levels (SpO2 ≤ 94.5%), high levels (96.5% < SpO2 ≤ 98.5%), and notably high levels (>98.5%). Subgroup analysis demonstrated no significant interaction between SpO2 and grouping variables, including Sex, Age, Congestive heart failure, Temperature, and ICU length of stay (LOS-ICU; P-values for interaction were >0.05).ConclusionsStriking an optimal balance is paramount, as fixating solely on lower SpO2 limits or neglecting high SpO2 levels may contribute to increased mortality rates. To mitigate mortality risk in elderly T2DM patients with cerebral infarction, we recommend maintaining SpO2 levels within the range of 94.5–96.5%.

show abstract

“…Recent studies demonstrate a role for miR-181c-5p in cardiovascular physiology, but its multi-organ crosstalk is understudied (19)(20)(21)(22)(23). In the heart, overexpression of miR-181c-5p is associated with enhanced propensity for HF development and cardiac damage (24)(25)(26)(27)(28).…”

Section: Introductionmentioning

confidence: 99%

Divergent cardiac and renal effects of miR-181c-5p inhibition in a rodent heart failure model

Boen,

Gevaert,

Dendooven

et al. 2024

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

AimsMiR-181c-5p overexpression associates with heart failure (HF) and cardiac damage, but the underlying pathophysiology remains unclear. This study investigated the effect of miR-181c-5p inhibition on cardiac function and fibrosis in a rodent model of diastolic dysfunction, and evaluated additional effects on kidney as relevant comorbid organ.Methods and resultsDiastolic dysfunction was induced in male C57/BL6J mice (n = 20) by combining high-fat diet, L-NG-nitroarginine methyl ester, and angiotensin II administration, and was compared to sham controls (n = 18). Mice were randomized to subcutaneous miR-181c-5p antagomiR (INH) or scrambled antagomiR injections (40 mg/kg/week). HF mice demonstrated diastolic dysfunction and increased fibrosis, which was attenuated by INH treatment. Remarkably, HF + INH animals had a threefold higher mortality rate (60%) compared to HF controls (20%). Histological examination revealed increased glomerular damage in all INH treated mice, and signs of thrombotic microangiopathy (TMA) in mice who died prematurely. Quantitative polymerase chain reaction demonstrated a miR-181c-5p-related downregulation of cardiac but not renal Tgfbr1 in HF + INH mice, while INH treatment reduced renal but not cardiac Vegfa expression in all mice.ConclusionThis study demonstrates cardiac anti-fibrotic effects of miR-181c-5p inhibition in a rodent HF model through targeting of Tgfbr1 in the heart. Despite improved diastolic function, HF + INH mice had higher mortality due to increased predisposition for TMA, increased renal fibrosis and glomerular damage, associated with Vegfa downregulation in kidneys.

show abstract

miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

Cited by 6 publications

References 48 publications

Long noncoding RNA ANRIL alleviates hypoxia‐induced pulmonary microvascular endothelial cell damage

Long noncoding RNA ANRIL alleviates hypoxia‐induced pulmonary microvascular endothelial cell damage

Association between SpO2 and the risk of death in elderly T2DM patients with cerebral infarction: a retrospective cohort study

Divergent cardiac and renal effects of miR-181c-5p inhibition in a rodent heart failure model

Contact Info

Product

Resources

About