miR-106b suppresses pathological retinal angiogenesis

Ménard, Catherine; Wilson, Ariel M.; Dejda, Agnieszka; Miloudi, Khalil; Binet, François; Crespo-Garcia, Sergio; Parinot, Célia; Pilon, Frédérique; Juneau, Rachel; Andriessen, Elisabeth M M A; Mawambo, Gaëlle; SanGiovanni, John Paul; Guire, Vincent De; Sapieha, Przemysław

doi:10.18632/aging.202404

Cited by 8 publications

(8 citation statements)

References 49 publications

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“…Suppressed PERK expression in photoreceptors and RPE cells could rescue the retina from light damage [ 105 ]. PERK downregulation consistently promotes the expression of the miR-106b-25 cluster to prevent the retina from oxidative stress [ 106 ]. The hyperactivation of the IRE1α induced by ER stress contributes to cell death [ 107 ].…”

Section: Nrf2 Signalling In the Retinamentioning

confidence: 99%

The Role of Nrf2/sMAF Signalling in Retina Ageing and Retinal Diseases

Zhang

Zeng

et al. 2023

Biomedicines

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Age-related diseases, such as Parkinson’s disease, Alzheimer’s disease, cardiovascular diseases, cancers, and age-related macular disease, have become increasingly prominent as the population ages. Oxygen is essential for living organisms, but it may also cause disease when it is transformed into reactive oxygen species via biological processes in cells. Most of the production of ROS occurs in mitochondrial complexes I and III. The accumulation of ROS in cells causes oxidative stress, which plays a crucial role in human ageing and many diseases. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a key antioxidant transcription factor that plays a central role in many diseases and ageing in general. It regulates many downstream antioxidative enzymes when cells are exposed to oxidative stress. A basic-region leucine zipper (bZIP) transcription factor, MAF, specifically the small MAF subfamily (sMAFs), forms heterodimers with Nrf2, which bind with Maf-recognition elements (MAREs) in response to oxidative stress. The role of this complex in the human retina remains unclear. This review summarises the current knowledge about Nrf2 and its downstream signalling, especially its cofactor—MAF, in ageing and diseases, with a focus on the retina. Since Nrf2 is the master regulator of redox homeostasis in cells, we hypothesise that targeting Nrf2 is a promising therapeutic approach for many age-related diseases.

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Section: Nrf2 Signalling In the Retinamentioning

confidence: 99%

The Role of Nrf2/sMAF Signalling in Retina Ageing and Retinal Diseases

Zhang

Zeng

et al. 2023

Biomedicines

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“…In ECs, miR-106b was shown to have anti-angiogenic effects through inhibiting STAT3 [68]. VEGFA expression is likewise affected by miR-106b [69], with upregulation of VEGFA in choroid specimens being stimulated by reduced miR-106b [36]. IPA predictions support these findings by demonstrating that upregulated miR-106b-3p leads to the predicted indirect inhibition of STAT3 and VEGFA leads to indirect activation of CVD.…”

Section: Upregulation Of Mir-106b-3p Expression In T1dmmentioning

confidence: 81%

“…There is not currently unanimous agreement on the role of miR-106b-3p in cardiovascular pathology, but various studies show its involvement in mechanisms related to CVD. Studies have also associated its precursor miR-106b with suppression of cell proliferation [59] and angiogenesis [36].…”

Section: Upregulation Of Mir-106b-3p Expression In T1dmmentioning

confidence: 99%

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Upregulation of Anti-Angiogenic miR-106b-3p Correlates Negatively with IGF-1 and Vascular Health Parameters in a Model of Subclinical Cardiovascular Disease: Study with Metformin Therapy

Bakhashab,

O’Neill,

Barber

et al. 2024

Biomedicines

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Well-controlled type 1 diabetes mellitus (T1DM) is regarded as a model of subclinical cardiovascular disease (CVD), characterized by inflammation and adverse vascular health. However, the underlying mechanisms are not fully understood. We investigated insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 (IGFBP-3) levels, their correlation to miR-106b-3p expression in a subclinical CVD model, and the cardioprotective effect of metformin. A total of 20 controls and 29 well-controlled T1DM subjects were studied. Plasma IGF-1, IGFBP-3 levels, and miR-106b-3p expression in colony-forming unit-Hills were analyzed and compared with vascular markers. miR-106b-3p was upregulated in T1DM (p < 0.05) and negatively correlated with pro-angiogenic markers CD34+/100-lymphocytes (p < 0.05) and IGF-1 (p < 0.05). IGF-1 was downregulated in T1DM (p < 0.01), which was associated with increased inflammatory markers TNF-α, CRP, and IL-10 and reduced CD34+/100-lymphocytes. IGFBP-3 had no significant results. Metformin had no effect on IGF-1 but significantly reduced miR-106b-3p (p < 0.0001). An Ingenuity Pathway analysis predicted miR-106b-3p to inhibit PDGFA, PIK3CG, GDNF, and ADAMTS13, which activated CVD. Metformin was predicted to be cardioprotective by inhibiting miR-106b-3p. In conclusion: Subclinical CVD is characterized by a cardio-adverse profile of low IGF-1 and upregulated miR-106b-3p. We demonstrated that the cardioprotective effect of metformin may be via downregulation of upregulated miR-106b-3p and its effect on downstream targets.

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“…It down-regulates the expression of VEGFA and HIF1α. Moreover, it prevents migration of human retinal microvascular endothelial cells and sprouting—cellular processes involved in angiogenesis [ 33 ]. miR-93 represses angiogenesis by reducing mRNA and protein expression of VEGF and decreasing human microvascular-endothelial-cell proliferation.…”

Section: Influence Of Mirnas On Angiogenesis In Amd Pathogenesismentioning

confidence: 99%

The Role of Dysregulated miRNAs in the Pathogenesis, Diagnosis and Treatment of Age-Related Macular Degeneration

Urbańska

Stępień

Nowakowska

et al. 2022

IJMS

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Age-related macular degeneration (AMD) is an eye disease causing damage to the macular region of the retina where most of the photoreceptors responsible for central visual acuity are located. MicroRNAs (miRNAs) are small single-stranded non-coding RNA molecules that negatively regulate genes by silent post-transcriptional gene expressions. Previous studies have shown that changes in specific miRNAs are involved in the pathogenesis of eye diseases, including AMD. Altered expressions of miRNAs are related to disturbances of regulating oxidative stress, inflammation, angiogenesis, apoptosis and phagocytosis, which are known factors in the pathogenesis of AMD. Moreover, dysregulation of miRNA is involved in drusen formation. Thus, miRNAs may be used as potential molecular biomarkers for the disease and, furthermore, tailoring therapeutics to particular disturbances in miRNAs may, in the future, offer hope to prevent irreversible vision loss. In this review, we clarify the current state of knowledge about the influence of miRNA on the pathogenesis, diagnosis and treatment of AMD. Our study material consisted of publications, which were found in PubMed, Google Scholar and Embase databases using “Age-related macular degeneration”, “miRNA”, “AMD biomarkers”, “miRNA therapeutics” and “AMD pathogenesis” as keywords. Paper search was limited to articles published from 2011 to date. In the section “Retinal, circulating and vitreous body miRNAs found in human studies”, we limited the search to studies with patients published in 2016–2021.

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miR-106b suppresses pathological retinal angiogenesis

Cited by 8 publications

References 49 publications

The Role of Nrf2/sMAF Signalling in Retina Ageing and Retinal Diseases

The Role of Nrf2/sMAF Signalling in Retina Ageing and Retinal Diseases

Upregulation of Anti-Angiogenic miR-106b-3p Correlates Negatively with IGF-1 and Vascular Health Parameters in a Model of Subclinical Cardiovascular Disease: Study with Metformin Therapy

The Role of Dysregulated miRNAs in the Pathogenesis, Diagnosis and Treatment of Age-Related Macular Degeneration

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