- Adipose Tissue-Derived Stem Cells
- Human Neurons
- Mouse Probe
- Whole Chromosome Painting Probes
- Hepatic Cells
- Renal Cells
- In Vitro ADME Kits
- Tissue Microarray
- Tissue Blocks
- Tissue Sections
- FFPE Cell Pellet
- Probe
- Centromere Probes
- Telomere Probes
- Satellite Enumeration Probes
- Subtelomere Specific Probes
- Bacterial Probes
- ISH/FISH Probes
- Exosome Isolation Kit
- Human Adult Stem Cells
- Mouse Stem Cells
- iPSCs
- Mouse Embryonic Stem Cells
- iPSC Differentiation Kits
- Mesenchymal Stem Cells
- Immortalized Human Cells
- Immortalized Murine Cells
- Cell Immortalization Kit
- Adipose Cells
- Cardiac Cells
- Dermal Cells
- Epidermal Cells
- Peripheral Blood Mononuclear Cells
- Umbilical Cord Cells
- Monkey Primary Cells
- Mouse Primary Cells
- Breast Tumor Cells
- Colorectal Tumor Cells
- Esophageal Tumor Cells
- Lung Tumor Cells
- Leukemia/Lymphoma/Myeloma Cells
- Ovarian Tumor Cells
- Pancreatic Tumor Cells
- Mouse Tumor Cells
Our Promise to You
Guaranteed product quality, expert customer support
MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway
PMID:30015903
Abstract
BACKGROUND: Intracranial aneurysm (IA) is an abnormal expansion in the intracranial arteries that weakens the arterial wall by consistently pushing the vascular wall outwards, which leads to a higher risk of aneurysm rupture. A number of reports have demonstrated that apoptosis is associated with the growth and rupture of IA. MicroRNAs (miRNAs/miRs) perform vital roles in the regulation of the mitochondrial apoptotic pathway and signaling proteins. Increasing evidence has already revealed the role of miR‑29a in injury, including liver injury, cardiovascular injury and ischaemia‑reperfusion injury. However, the role of miR‑29a in IA remains unclear at present.
METHODS: The present study investigated the role of miR‑29a in IA pathogenesis and the underlying mechanisms.
RESULTS: By using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, the present study demonstrated that genes, including caspase‑3, ‑8 and ‑9, and proteins, including cytochrome c and myeloid cell leukemia 1 (Mcl‑1), involved in mitochondrial apoptosis pathways were upregulated in IA groups compared with controls. In addition, microarray analysis demonstrated that miR‑29a, one of the most altered miRs in IA mice, was overexpressed in IA mice compared with controls. In vitro experiments revealed that miR‑29a downregulation attenuated human brain vascular smooth muscle cell (HBVSMC) apoptosis, while miR‑29a overexpression increased the apoptosis of HBVSMCs. Furthermore, luciferase reporter analysis revealed that Mcl‑1 is a direct target gene of miR‑29a. An in vivo IA model confirmed that miR‑29a overexpression may promote apoptosis through mitochondrial pathways.
CONCLUSION: It was therefore concluded that miR‑29a may contribute to the progression of IA by regulating mitochondrial apoptotic pathways. Thus, miR‑29a is a potential therapeutic target for IA.