Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury

Tang, Wei; Guo, Zongduo; Chai, Weina; Du, Donglin; Yang, Xingsheng; Cao, Lang; Chen, Hong; Zhou, Chao; Cheng, Chung–Ying; Sun, Xiaochuan; Huang, Zhijian; Zhong, Jian

doi:10.4103/1673-5374.314326

Cited by 16 publications

(7 citation statements)

References 57 publications

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“…By competitively binding with miR‐491‐5p, lncRNAs, such as lncRNA AK046375, LINC02381 and lncRNA LBX2‐AS1, can modulate the progression cancers and oxidative stress 41,42 . In addition, miR‐491‐5p exerts critical functions in fibrosis and oxidative stress 41,43–47 . For example, overexpression of miR‐491‐5p destroyed cell–cell connection, and elevated miR‐491‐5p expression induced by TGF‐β1 was involved in renal fibrosis 43 .…”

Section: Discussionmentioning

confidence: 99%

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LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Li,

Zou,

Jin

et al. 2024

Environmental Toxicology

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Liver fibrosis is an invertible pathophysiologic process featured by excessive accumulation of extracellular matrix (ECM) which injures liver cells and activates hepatic stellate cells (HSCs). Besides, inducing ferroptosis in activated HSCs can alleviate liver fibrosis. LncRNAs modulate ferroptosis in activated HSCs and ECM deposition in liver fibrosis. However, the role of lncRNA FRMD6‐AS1 in liver fibrosis is not discovered. In this study, lncRNA FRMD6‐AS1 was dramatically up‐regulated in activated HSCs. Knockdown of FRMD6‐AS1 markedly increased iron ion, ROS and MDA levels, decreased GSH level, SLC7A11 and GPX4 protein expressions in activated HSCs. In addition, HSCs activation markers α‐SMA and COL1α1 expressions were up‐regulated in activated HSCs; knockdown of FRMD6‐AS1 markedly down‐regulated α‐SMA and COL1α1 expressions in HSCs. Besides, lncRNA FRMD6‐AS1 could interact with miR‐491‐5p, and negatively modulate miR‐491‐5p expression. USP13 was a target of miR‐491‐5p, and could be negatively modulated by miR‐491‐5p. Moreover, FRMD6‐AS1 knockdown increased iron ion and ROS levels, decreased SLC7A11 and GPX4 protein expressions, facilitated HSCs viability, and up‐regulated α‐SMA and COL1α1 expressions via miR‐491‐5p/USP13 pathway. Finally, FRMD6‐AS1 knockdown restored liver tissue structure and abrogated fibrosis in livers in a CCL4 liver fibrosis mouse model. Hence, lncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway repressed ferroptosis, promoted ECM deposition and facilitated liver fibrosis in vitro and in vivo models.

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Section: Discussionmentioning

confidence: 99%

“…## p < .01 vs. PDGF-BB + si-NC. & p < .05, && p < .01 vs. PDGF-BB + si-FRMD6-AS1.critical functions in fibrosis and oxidative stress 41,[43][44][45][46][47]. For example, overexpression of miR-491-5p destroyed cell-cell connection, and elevated miR-491-5p expression induced by TGF-β1 was involved in renal fibrosis 43.…”

mentioning

confidence: 99%

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Li,

Zou,

Jin

et al. 2024

Environmental Toxicology

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“…MiR-491-5p promotes apoptosis. 63 Three brain-enriched miRNAs, miR-99b-5p, miR-127-3p and miR-181a-5p, were increased in stroke participants versus controls at 15 days poststroke in both cohorts and at 30 days in the discovery cohort. MiR-99b-5p acts to suppress cell proliferation.…”

Section: Brain-enriched Mirnasmentioning

confidence: 90%

Expansion of plasma MicroRNAs over the first month following human stroke

Edwardson,

Shivapurkar,

et al. 2023

J Cereb Blood Flow Metab

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Few have characterized miRNA expression during the transition from injury to neural repair and secondary neurodegeneration following stroke in humans. We compared expression of 754 miRNAs from plasma samples collected 5, 15, and 30 days post-ischemic stroke from a discovery cohort (n = 55) and 15-days post-ischemic stroke from a validation cohort (n = 48) to healthy control samples (n = 55 and 48 respectively) matched for age, sex, race and cardiovascular comorbidities using qRT-PCR. Eight miRNAs remained significantly altered across all time points in both cohorts including many described in acute stroke. The number of significantly dysregulated miRNAs more than doubled from post-stroke day 5 (19 miRNAs) to days 15 (50 miRNAs) and 30 (57 miRNAs). Twelve brain-enriched miRNAs were significantly altered at one or more time points (decreased expression, stroke versus controls: miR-107; increased expression: miR-99-5p, miR-127-3p, miR-128-3p, miR-181a-3p, miR-181a-5p, miR-382-5p, miR-433-3p, miR-491-5p, miR-495-3p, miR-874-3p, and miR-941). Many brain-enriched miRNAs were associated with apoptosis over the first month post-stroke whereas other miRNAs suggested a transition to synapse regulation and neuronal protection by day 30. These findings suggest that a program of decreased cellular proliferation may last at least 30 days post-stroke, and points to specific miRNAs that could contribute to neural repair in humans.

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“…Interestingly, at 3-months after the last mTBI, both proximal and distal ROIs had a lower AUC of the CBF during hypercapnia, whereas at 9-months after the last mTBI, only the proximal ROI had a lower AUC of the CBF during hypercapnia 38 . Furthermore, CCI-induced TBI resulted in a CBF reduction that coincided with reduced vascular density 207 . Notably, downregulating miR-491-5p, which is important in cell proliferation and migration, resulted in improved CBF, increased vascular density, better neurological function, and better survival of neurons after TBI.…”

Section: Applicationsmentioning

confidence: 95%

“… 38 Furthermore, CCI-induced TBI resulted in a CBF reduction that coincided with reduced vascular density. 207 Notably, downregulating miR-491-5p, which is important in cell proliferation and migration, resulted in improved CBF, increased vascular density, better neurological function, and better survival of neurons after TBI. In addition, TREM2 impacts the extent of injury following CCI-induced TBI.…”

Section: Applicationsmentioning

confidence: 99%

Intrinsic, widefield optical imaging of hemodynamics in rodent models of Alzheimer’s disease and neurological injury

et al. 2023

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. The complex cerebrovascular network is critical to controlling local cerebral blood flow (CBF) and maintaining brain homeostasis. Alzheimer’s disease (AD) and neurological injury can result in impaired CBF regulation, blood–brain barrier breakdown, neurovascular dysregulation, and ultimately impaired brain homeostasis. Measuring cortical hemodynamic changes in rodents can help elucidate the complex physiological dynamics that occur in AD and neurological injury. Widefield optical imaging approaches can measure hemodynamic information, such as CBF and oxygenation. These measurements can be performed over fields of view that range from millimeters to centimeters and probe up to the first few millimeters of rodent brain tissue. We discuss the principles and applications of three widefield optical imaging approaches that can measure cerebral hemodynamics: (1) optical intrinsic signal imaging, (2) laser speckle imaging, and (3) spatial frequency domain imaging. Future work in advancing widefield optical imaging approaches and employing multimodal instrumentation can enrich hemodynamic information content and help elucidate cerebrovascular mechanisms that lead to the development of therapeutic agents for AD and neurological injury.

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Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury

Cited by 16 publications

References 57 publications

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Expansion of plasma MicroRNAs over the first month following human stroke

Intrinsic, widefield optical imaging of hemodynamics in rodent models of Alzheimer’s disease and neurological injury

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