Long noncoding RNA H19 mediates neural stem/progenitor cells proliferation, differentiation and apoptosis through the p53 signaling pathway after ischemic stroke

Gan, Li; Liao, Susan; Tong, Yanqiu; Li, Weihan; Peng, Wanling; Deng, Shixiong

doi:10.1016/j.bbrc.2022.01.095

Cited by 11 publications

(9 citation statements)

References 45 publications

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“…These results implied that by inhibiting p53 signaling, H19 could support cell proliferation and differentiation after OGD/R. 105 LncRNA NEAT1 has also been demonstrated to be crucial in ischemic injury. 106 LncRNA NEAT1 activated the Wnt/catenin pathway by upregulating Wnt3a in a U2AF2-dependent manner.…”

Section: Serum Ncrna-based Risk Prediction For Strokementioning

confidence: 82%

“…In conclusion, overexpression of H19 caused p53 to become inactive, which aided NSPC differentiation, proliferation, and resistance to apoptosis. These results implied that by inhibiting p53 signaling, H19 could support cell proliferation and differentiation after OGD/R 105 . LncRNA NEAT1 has also been demonstrated to be crucial in ischemic injury 106 .…”

Section: Ncrnas‐based Therapy In Strokementioning

confidence: 83%

“…104 Upregulation of H19 promoted cell proliferation and differentiation while reversing OGD/R-induced NSC apoptosis. 105 Additionally, the upregulation of p53 prevented the effects of overexpressed H19 on NSPCs' proliferation, differentiation, and apoptosis. In conclusion, overexpression of H19 caused p53 to become inactive, which aided NSPC differentiation, proliferation, and resistance to apoptosis.…”

Section: Serum Ncrna-based Risk Prediction For Strokementioning

confidence: 99%

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The exo‐microRNA (miRNA) signaling pathways in pathogenesis and treatment of stroke diseases: Emphasize on mesenchymal stem cells (MSCs)

Farahmand,

Nabiuni,

Vafaei Mastanabad

et al. 2024

Cell Biochemistry & Function

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A major factor in long‐term impairment is stroke. Patients with persistent stroke and severe functional disabilities have few therapy choices. Long noncoding RNAs (lncRNAs) may contribute to the regulation of the pathophysiologic processes of ischemic stroke as shown by altered expression of lncRNAs and microRNA (miRNAs) in blood samples of acute ischemic stroke patients. On the other hand, multipotent mesenchymal stem cells (MSCs) increase neurogenesis, and angiogenesis, dampen neuroinflammation, and boost brain plasticity to improve functional recovery in experimental stroke models. MSCs can be procured from various sources such as the bone marrow, adipose tissue, and peripheral blood. Under the proper circumstances, MSCs can differentiate into a variety of mature cells, including neurons, astrocytes, and oligodendrocytes. Accordingly, the capability of MSCs to exert neuroprotection and also neurogenesis has recently attracted more attention. Nowadays, lncRNAs and miRNAs derived from MSCs have opened new avenues to alleviate stroke symptoms. Accordingly, in this review article, we examined various studies concerning the lncRNAs and miRNAs' role in stroke pathogenesis and delivered an overview of the therapeutic role of MSC‐derived miRNAs and lncRNAs in stroke conditions.

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Section: Serum Ncrna-based Risk Prediction For Strokementioning

confidence: 82%

Section: Ncrnas‐based Therapy In Strokementioning

confidence: 83%

Section: Serum Ncrna-based Risk Prediction For Strokementioning

confidence: 99%

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The exo‐microRNA (miRNA) signaling pathways in pathogenesis and treatment of stroke diseases: Emphasize on mesenchymal stem cells (MSCs)

Farahmand,

Nabiuni,

Vafaei Mastanabad

et al. 2024

Cell Biochemistry & Function

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“…When Caspase-3 is stimulated by apoptosis, it is activated and cleaved into cleaved Caspase-3, an essential condition for the initiation of apoptosis (83). Subsequently, cleaved Caspase-3 will decompose the nuclear DNA repair enzymes, resulting in nuclear DNA chromatin condensation and damage, eventually leading to apoptosis (83)(84)(85).…”

Section: Discussionmentioning

confidence: 99%

Para‑hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation

et al. 2022

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Gastrodia elata (GE) Blume has been widely used for thousands of years to treat various central and peripheral nervous disorders. P-hydroxybenzaldehyde (PHBA) is a chemical component of GE. However, its role and mechanism in transient focal cerebral ischemia remain unclear. The present study aimed to investigate the protective effect of PHBA on middle cerebral artery occlusion (MCAO) rats. A total of 56 Sprague-Dawley male rats were randomly divided into control, model, PHBA-high dose (PHBA-H) and PHBA-low dose (PHBA-L) groups. The MCAO injury model was replicated in all rats except for the control group. In the control group, only the right common carotid artery was isolated without embolization. After treatment with PHBA, the protective effects (neurological deficit score, cerebral index, weight and cerebral infarct) were analyzed. Western blotting was performed to estimate the protein levels of Bcl-2, Bax and Caspase-3. Apoptotic cells were detected using hematoxylin-eosin staining and TUNEL immunofluorescence assay. Mitochondrial oxidative stress indicators, including reactive oxygen species (ROS), malondialdehyde (MDA) and total superoxide dismutase (T-SOD), while dysfunction indicators, including mitochondrial permeability transition pore (MPTP), ATP and cytochrome C oxidase, were measured using commercial kits. The ultrastructure of mitochondria was observed under an electron microscope. Once the model was successful established, the rats in the MCAO group suffered neurological damage (P<0.001), increased cerebral index (P<0.001), decreased body weight (P<0.001) and had severe cerebral infarction (P<0.001). Moreover, the number of apoptotic cells and the levels of ROS (P<0.001) and MDA (P<0.05) in mitochondria and the protein levels of Bax (P<0.001) and cleaved caspase-3 (P<0.001) were increased. The activities of T-SOD (P<0.001) and cytochrome C oxidase (P<0.001) in the mitochondria, ATP content (P<0.05) and Bcl-2 protein level (P<0.001) decreased, MPTP was stimulated to open and mitochondrial structures were damaged (P<0.001). PHBA treatment resulted in a decrease of the neurological deficit score (PHBA-H 24 h, P<0.001; PHBA-H 6 h and PHBA-L 24 h, P<0.01; PHBA-L 6 h, P<0.05), apoptotic cell number (P<0.001), mitochondrial ROS (P<0.001) and MPTP opening (P<0.001), Bax (P<0.01, P<0.001) and cleaved caspase-3 protein expression (P<0.001) in rats. And the expression of Bcl-2 protein (P<0.001) was increased. In addition, the cerebral index (P<0.05), weight loss (P<0.05), infarction rate (P<0.01) and MDA content (P<0.001) were decrease in the PHBA-H group. The level of ATP (P<0.05) and cytochrome C oxidase (P<0.05) and T-SOD activity (P<0.05) of PHBA-H group rats increased, but no significant difference was observed in the PHBA-L group. Overall, PHBA had a protective effect on transient focal cerebral ischemia in normal rats, regulated the expression of Bcl-2, Bax and cleaved caspase-3 proteins and improved the oxidative stress and dysfunction of mitochondria.

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“…Knotek et al ( 30 ) demonstrated that Wnt signaling regulated the biological function of NSPCs and could be considered useful in ischemic stroke therapy. Gan et al ( 31 ) indicated that long noncoding RNA H19 promoted NSPCs proliferation and differentiation via the p53 signaling pathway. During an ischemic stroke, due to damage to the blood-brain barrier, excitotoxicity and neuroinflammation destroy the cellular microenvironment to a great extent ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

Artesunate regulates the proliferation and differentiation of neural stem cells by activating the JAK‑2/STAT‑3 signaling pathway in ischemic stroke

2022

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Ischemic stroke is one of the most common causes of disability and death globally; therefore, the repair and reconstruction of the central nervous system (CNS) after stroke is very important. Neural stem/progenitor cells (NSPCs) may be the key to cell replacement therapy to treat CNS damage. It has previously been reported that artesunate (ART) is involved in the regulation of the biological functions of NSPCs; however, the mechanism of action of ART remains unclear. In the present study, different concentrations of ART were used to treat NSPCs following oxygen-glucose deprivation (OGD). Cell viability and apoptosis were analyzed using Cell Counting Kit-8 assay and flow cytometry, respectively, whereas immunofluorescence analysis was used to measure the expression levels of the differentiation-related molecule doublecortin (DCX) and proliferating cell nuclear antigen (PCNA). Western blotting was performed to analyze the expression levels of molecules related to the JAK-2/STAT-3 signaling pathway. The present results indicated that treatment with ART following OGD significantly promoted the viability of NSPCs, inhibited the apoptosis of NSPCs, and promoted the expression of PCNA and DCX. Moreover, ART significantly downregulated the protein expression levels of phosphorylated (p)-JAK-2 and p-STAT-3. Furthermore, activation of the JAK-2/STAT-3 signaling pathway and treatment with ART reversed the effects of ART on the proliferation, apoptosis and differentiation of NSPCs. In conclusion, the present data suggested that ART may promote the proliferation and differentiation of NSPCs, and reduce the apoptosis of NSPCs, by inhibiting the JAK-2/STAT-3 signaling pathway. ART may potentially be used for the treatment of ischemic stroke.

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Long noncoding RNA H19 mediates neural stem/progenitor cells proliferation, differentiation and apoptosis through the p53 signaling pathway after ischemic stroke

Cited by 11 publications

References 45 publications

The exo‐microRNA (miRNA) signaling pathways in pathogenesis and treatment of stroke diseases: Emphasize on mesenchymal stem cells (MSCs)

The exo‐microRNA (miRNA) signaling pathways in pathogenesis and treatment of stroke diseases: Emphasize on mesenchymal stem cells (MSCs)

Para‑hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation

Artesunate regulates the proliferation and differentiation of neural stem cells by activating the JAK‑2/STAT‑3 signaling pathway in ischemic stroke

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