miR-34a regulates phenotypic modulation of vascular smooth muscle cells in intracranial aneurysm by targeting CXCR3 and MMP-2

Yuan, Xuesong; Bian, Xiaoxing; Wei, Wei; Bao, Qing; Liu, Ping; Jiang, Wenqing

doi:10.1590/1678-4685-gmb-2020-0124

Cited by 5 publications

(4 citation statements)

References 27 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is evidence that HDAC9 is enriched at the miR-20a promoter and inhibits miR-20a expression [ 32 ]. It has been reported that miR-34a is regulated by HDAC1 and downregulated at IA [ 19 , 20 ]. In view of this, we speculated that miR-34a-5p is involved in the downstream mechanism of HDAC9.…”

Section: Resultsmentioning

confidence: 99%

“…Our data suggest that HDAC9 is enriched at the miR-34a promoter and can reduce the enrichment of H3K9ac, H3K14ac, and H3K18ac at the promoter, resulting in decreased miR-34a-5p expression. A pioneering study has documented the involvement of miR-34a in the phenotypic regulation of VSMCs to influence progression IA [ 19 ]. Since VSMCs can induce the functional change of VECs [ 38 ], miR-34a could also regulate the functions of VECs.…”

Section: Discussionmentioning

confidence: 99%

“…miR-34a has been documented as a miR signature for tumorigenesis, neuropathology, and immunomodulation [ 16–18 ]. Interestingly, miR-34a has been shown to be decreased in IA and regulate IA progression through phenotypic modulation of VSMCs [ 19 ]. Previous studies have reported that the depletion of HDAC1 leads to the upregulation of miR-34a [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Aberrant expression and regulatory role of histone deacetylase 9 in vascular endothelial cell injury in intracranial aneurysm

Sun¹,

ZHANG²,

Cheng³

et al. 2023

Biomol Biomed

View full text Add to dashboard Cite

Intracranial aneurysm (IA) is one of the most challenging cerebrovascular lesions for clinicians. The aim of this study was to investigate the abnormal expression and role of histone deacetylase 9 (HDAC9) in IA-associated injury of vascular endothelial cells (VECs). First, IA tissue and normal arterial tissue were collected and VECs were isolated from IA patients. The expression levels of HDAC9, microRNA (miR)-34a-5p, and vascular endothelial growth factor-A (VEGFA) were determined. Cell viability, proliferation, apoptosis, and migration were assessed by Cell Counting Kit-8 (CCK-8) assay, EdU staining, TUNEL staining, and transwell assay. The binding of miR-34a-5p to VEGFA was analyzed by the dual-luciferase assay, and the accumulation of HDAC9 and lysine histone acetylation at H3 (H3K9, H3K14, and H3K18) on the miR-34a-5p promoter was detected by the chromatin immunoprecipitation assay. The results showed that HDAC9 and VEGFA were increased and miR-34a-5p was decreased in IA tissues and cells. Silencing of HDAC9 inhibited apoptosis and increased viability, proliferation, and migration of VECs, whereas overexpression of HDAC9 exerted the opposite functions. HDAC9 accumulated at the miR-34a-5p promoter to decrease miR-34a-5p expression by reducing H3 locus-specific acetylation and further promoted VEGFA expression. Knockdown of miR-34a-5p or VEGFA overexpression reversed the protective role of HDAC9 silencing in VECs injury. In conclusion, our study suggests that HDAC9 may be a therapeutic target for IA.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Aberrant expression and regulatory role of histone deacetylase 9 in vascular endothelial cell injury in intracranial aneurysm

Sun¹,

ZHANG²,

Cheng³

et al. 2023

Biomol Biomed

View full text Add to dashboard Cite

show abstract

“…Currently, there is evidence that there is a biological link between miRNA and IA. For instance, miR-34a modulates phenotypic modulation of VSM cells via CXCR3 and MMP-2 in IA [ 5 ]. miR-21 participated in the formation of intracranial aneurysm through JNK signaling [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

miR-139-5p Suppresses Proliferation and Angiogenesis of Intracranial Aneurysm via FGB

Jin

Chen

et al. 2022

Journal of Healthcare Engineering

View full text Add to dashboard Cite

Intracranial aneurysm (IA) is a common cerebrovascular disease. Understanding the mechanism regulating the progression of IA could help to develop novel therapeutic methods for this disease. In this study, we confirmed FGB is one of the targets of miR-139-5p. Moreover, miR-139-5p expression in intracranial aneurysm specimens was suppressed compared with normal tissues. However, we found that FGB in intracranial aneurysm samples was remarkedly enhanced compared to normal tissues. Moreover, we found miR-139-5p overexpression and FGB silencing inhibit HBMEC proliferation and tube formation and suppressed α-SMA and CXCR4 levels in HBMEC cells. Furthermore, a rescue experiment confirmed miR-139-5p affected the proliferation and angiogenesis of HBMEC through FGB. Despite further research being needed to determine the exact functions of miR-139-5p in the formation of CA, our new findings contribute to a comprehensive understanding of the treatment mechanism of IA.

show abstract

Effects of KLF11 on Vascular Smooth Muscle Cells and its Underlying Mechanisms in Intracranial Aneurysm

Yan,

Bian,

et al. 2024

Biochem Genet

View full text Add to dashboard Cite

miR-34a regulates phenotypic modulation of vascular smooth muscle cells in intracranial aneurysm by targeting CXCR3 and MMP-2

Cited by 5 publications

References 27 publications

Aberrant expression and regulatory role of histone deacetylase 9 in vascular endothelial cell injury in intracranial aneurysm

Aberrant expression and regulatory role of histone deacetylase 9 in vascular endothelial cell injury in intracranial aneurysm

miR-139-5p Suppresses Proliferation and Angiogenesis of Intracranial Aneurysm via FGB

Effects of KLF11 on Vascular Smooth Muscle Cells and its Underlying Mechanisms in Intracranial Aneurysm

Contact Info

Product

Resources

About