Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis

Chen, Bing; Wang, Haoran; Lv, Chen; Mao, Chongdan; Cui, Yuguang

doi:10.1080/21655979.2021.1951070

Cited by 40 publications

(40 citation statements)

References 44 publications

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“…As a “star molecule,” lncRNA H19 has been manifested that its downregulation can reduce brain edema and alleviate brain damage as well as neurological injury when ischemia occurs [ 13 ]. Chen et al [ 14 ] showed for the first time that lncRNA H19 expression was upregulated in ICH cell model. And lncRNA H19 downregulation could promote the proliferation of brain microvascular endothelial cells and inhibit ferroptosis, thus achieving the effect of treating ICH.…”

Section: Introductionmentioning

confidence: 99%

lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-κB Pathway

Mao

Huang

Chen

2022

Computational and Mathematical Methods in Medicine

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Objective. To explore the effect of long noncoding RNA H19 (lncRNA H19) on brain injury in rats following experimental intracerebral hemorrhage (ICH). Methods. Rat ICH model was established with type IV collagenase. The neurological function scores were evaluated, and the water content in brain tissue was measured. The nerve injury indexes, inflammatory factors, and oxidative stress indexes were also measured. Moreover, the expression of lncRNA H19 was determined by qRT-PCR, and Western blot detected NF-κB pathway-related protein expression. Results. Compared with the sham group, the neurological function scores, the water content in brain tissue, and levels of injury indicators myelin basic protein (MBP), S-100B, and neuron-specific enolase (NSE) in the ICH rats were significantly increased. Meanwhile, the levels of TNF-α, IL-6, IL-1β, ROS, and MDA were significantly increased, but the levels of SOD were significantly decreased. In addition, the expression of lncRNA H19 in the brain tissue in the ICH group was significantly higher than that in the sham group. After further interference with lncRNA H19 expression (sh-H19 group), the levels of all the above indicators were reversed and the neurological damage was improved. Western blot results showed that the expression of NF-κBp65 and IKKβ was significantly higher, and IκBα expression was lower in the perivascular hematoma tissue in the ICH group compared with the sham group. Compared with the sh-NC group, NF-κBp65 and IKKβ expression were significantly lower and IκBα was significantly higher in the sh-H19 group. Conclusion. lncRNA H19 exacerbated brain injury in rats with ICH by promoting neurological impairment, brain edema, and releasing inflammatory responses and oxidative stress. This may be related to the activation of NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-κB Pathway

Mao

Huang

Chen

2022

Computational and Mathematical Methods in Medicine

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“…The expression of lncRNA H19 in brain tissues was upregulated after intracerebral hemorrhage (ICH), which could activate NF-κB and enhance inflammatory responses to aggravate brain edema and neurological injury [ 54 , 55 ]. The role of lncRNA Mir155hg in brain injury has rarely been reported.…”

Section: Discussionmentioning

confidence: 99%

Construction of a lncRNA-associated competing endogenous RNA regulatory network after traumatic brain injury in mouse

Wang

Sun

et al. 2022

Mol Brain

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Traumatic brain injury (TBI) is a major public health problem worldwide which causes high mortality and disability. Functioning as microRNA (miRNA) sponges, long non-coding RNA (lncRNA) regulates the expression of protein-coding genes in a competing endogenous RNA (ceRNA) network. However, the lncRNA-associated ceRNA in TBI remains unclear. In this study, we processed the raw SRR files of mice cortex samples of sham injury (n = 3) and TBI groups (n = 3) to count files. Then, the expression profiles of lncRNAs and mRNAs were identified, and 86 differentially expressed (DE) lncRNAs and 1201 DEmRNAs between sham and TBI groups were identified. The DEmRNAs were used to perform enrichment analyses. Next, a lncRNA-miRNA-mRNA regulatory ceRNA network was constructed. The network consisted of 23 mRNAs, 5 miRNAs and 2 lncRNAs. The expression alternations of the 5 miRNAs were validated via qRT-PCR. The subnetwork of hub lncRNA Neat1 was extracted. We identified a potential inflammatory associated regulatory axis: Neat1/miR-31-5p/Myd88 axis. The PPI network based on DEmRNA involved in ceRNA network was constructed PPI networks to identify the hub genes. Finally, DElncRNAs and DEmRNAs were selected randomly and validated by qRT-PCR. In conclusion, with the lncRNA-miRNA-mRNA ceRNA network provided above, we can improve our understanding of the regulatory mechanisms and interaction among lncRNAs, miRNAs and mRNAs in TBI process.

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“…ACSL4 is essential to execute ferroptosis by inducing 5-hydroxyeicosatetraenoic acid production [ 112 ] and enriching cellular membranes with long polyunsaturated ω6 fatty acids [ 13 ]. It has been shown that ACSL4 is a target of miR-106b-5p in brain microvascular endothelial cells [ 61 ], and miR-106 has been demonstrated to enhance radiation sensitivity of head and neck cancers [ 62 ]. Additionally, ACSL4 was also under the control of miR-424-5p in ovarian cancer [ 63 ].…”

Section: Ferroptosis-associated Non-coding Rnas In Head and Neck Cancersmentioning

confidence: 99%

Regulation of Ferroptosis by Non-Coding RNAs in Head and Neck Cancers

Hsieh

Chao

Chu

et al. 2022

IJMS

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Ferroptosis is a newly identified mode of programmed cell death characterized by iron-associated accumulation of lipid peroxides. Emerging research on ferroptosis has suggested its implication in tumorigenesis and stemness of cancer. On the other hand, non-coding RNAs have been shown to play a pivotal role in the modulation of various genes that affect the progression of cancer cells and ferroptosis. In this review, we summarize recent advances in the theoretical modeling of ferroptosis and its relationship between non-coding RNAs and head and neck cancers. Aside from the significance of ferroptosis-related non-coding RNAs in prognostic relevance, we also review how these non-coding RNAs participate in the regulation of iron, lipid metabolism, and reactive oxygen species accumulation. We aim to provide a thorough grounding in the function of ferroptosis-related non-coding RNAs based on current knowledge in an effort to develop effective therapeutic strategies for head and neck cancers.

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Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis

Abstract: 2021) Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis, Bioengineered, 12:1, 4004-4015,

Cited by 40 publications

References 44 publications

lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-κB Pathway

lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-κB Pathway

Construction of a lncRNA-associated competing endogenous RNA regulatory network after traumatic brain injury in mouse

Regulation of Ferroptosis by Non-Coding RNAs in Head and Neck Cancers

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