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lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: Jan 7, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
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Long Non-Coding RNA PVT1 Inhibits Apoptosis Through the miR-30d-5p/CaMKIIδ Axis in Hypoxic-Ischemic Brain Injury.

Fengyan Zhao1, Junyan Liu2, Zihong Xiong3

  • 1Department of Pediatrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), NHC Key Laboratory of Chronobiology, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.

Molecular Neurobiology
|December 8, 2025
PubMed
Summary
This summary is machine-generated.

Long noncoding RNA PVT1 protects against hypoxic-ischemic brain damage (HIBD) by regulating neuronal apoptosis. PVT1 acts as a sponge for miR-30d-5p, modulating CaMKIIδ expression to reduce brain injury.

Keywords:
ApoptosisBrain injuryHypoxic-ischemicNeuronNon-coding RNAs

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • MicroRNA-30d-5p (miR-30d-5p) plays a role in neuronal apoptosis following hypoxia-ischemia.
  • The precise molecular mechanisms of miR-30d-5p in hypoxic-ischemic brain damage (HIBD) are not fully understood.

Purpose of the Study:

  • To elucidate the mechanisms by which miR-30d-5p influences neuronal apoptosis in neonatal mice with HIBD and primary neurons subjected to oxygen-glucose deprivation (OGD).
  • To investigate the role of long noncoding RNA PVT1 (lncRNA PVT1) in the context of HIBD and its interaction with miR-30d-5p.

Main Methods:

  • RNA sequencing (RNA-seq) to identify differentially expressed lncRNAs.
  • Fluorescence in situ hybridization (FISH) and immunofluorescence staining to determine lncRNA PVT1 localization and expression.
  • In vivo studies in neonatal mice with HIBD and in vitro studies using primary neurons exposed to OGD.
  • Manipulation of lncRNA PVT1 and miR-30d-5p levels to assess effects on neuronal apoptosis, brain injury, and related molecular pathways.

Main Results:

  • RNA-seq identified lncRNA PVT1 as highly differentially expressed and predicted to bind miR-30d-5p.
  • lncRNA PVT1 expression increased in neurons after HIBD or OGD.
  • PVT1 inhibition exacerbated OGD-induced neuronal apoptosis and brain injury, while PVT1 overexpression showed neuroprotective effects.
  • PVT1 upregulated CaMKIIδ by sponging miR-30d-5p, affecting GSK3β phosphorylation and neuronal apoptosis.

Conclusions:

  • lncRNA PVT1 acts as a neuroprotective factor in hypoxia-ischemia-induced brain injury.
  • The PVT1/miR-30d-5p/CaMKIIδ axis is a key pathway regulating neuronal apoptosis in HIBD.
  • Targeting the PVT1/miR-30d-5p/CaMKIIδ pathway may offer therapeutic strategies for HIBD.