Expression of miR‑34a in cataract rats and its related mechanism

Xiu, Caimei; Jiang, Jing; Song, Ruiying

doi:10.3892/etm.2019.8295

Cited by 6 publications

(6 citation statements)

References 21 publications

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“…As an miRNA member, prior studies have indicated that miR-34a is deregulated in various cancers ( Li et al ., 2019 ; Liu et al ., 2020 ; Xiu et al ., 2020 ). Besides, it is the first miRNA found to be directly regulated by p53 ( Rokavec et al ., 2014 ).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

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Section: Discussionmentioning

confidence: 99%

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

et al. 2021

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“…They may exist in a stable state within cells or outside cells in biological fluids, including plasma and aqueous humor (AH), vitreous humor, serum, saliva, urine, and tears, and can exist as exosomes or be bound to carrier proteins [20,21]. Previous studies have reported that the expression of miRNAs can be involved in senescence or age-related neurological disorders, diabetes, degenerative arthritis, carcinomas, and cataracts [16,[21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37]. In glaucoma, miRNAs can regulate ECM metabolism by regulating TGF-β and can regulate stiffness by the accelerated maturation of ECM proteins, altering the trabecular meshwork (TM) contractile properties, thus accelerating or inhibiting TM cell senescence, or by modulating oxidative-and mechanical-stress-induced damage [20,22,38] in the cell/tissue(Table 1).…”

Section: Potential Role Of Mirnas In Xfgmentioning

confidence: 99%

Alternate Causes for Pathogenesis of Exfoliation Glaucoma, a Multifactorial Elastotic Disorder: A Literature Review

Chakraborty

Rao

2022

CIMB

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Exfoliation glaucoma (XFG) is the most recognizable form of secondary open-angle glaucoma associated with a high risk of blindness. This disease is characterized by white flaky granular deposits in the anterior chamber that leads to the elevation of intraocular pressure (IOP) and subsequent glaucomatous optic nerve damage. Conventionally, XFG is known to respond poorly to medical therapy, and surgical intervention is the only management option in most cases. Various genetic and nongenetic factors are known to be linked to the development of XFG. Despite decades of research on the genetic factors in exfoliation syndrome (XFS) by study groups and global consortia involving different ethnic populations, the pathogenesis of XFS and the mechanism of onset of glaucoma still remains an unsolved mystery. The key lies in understanding how the function of a gene (or set of genes) is altered by environmental triggers, along with other molecular events that underlie the key disease attributes, namely, oxidative stress and the disruption of the blood–aqueous barrier (BAB). It remains a challenge to evolve a theory encompassing all factions of molecular events occurring independently or parallelly that determine the disease manifestation (phenotype) or the stage of the disease in the eye (or in any tissue) in exfoliation. Our enhanced understanding of the underlying molecular pathophysiology of XFG, beyond the known genes or polymorphisms involved in the disease, will lead to improved diagnosis and management and the ability to recognize how the environment influences these key events that lead to the disease phenotype or disease progression. This review summarizes the recent observations and discoveries of four key factors that may hold the answers to the non-lysyl oxidase-like 1 (LOXL1) mechanisms behind XFG pathogenesis, namely, the epigenetic factor miRNA, disordered autophagy along with the potential involvement of mitochondrial mutations, and a compromised aqueous–blood barrier.

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“…Moreover, it inhibits cell death following DNA injury by antagonizing p53 acetylation (27). The upregulation of miRNA-34a expression level is associated with cataract occurrence in rats, which may be caused by down-regulation of Sirt1 protein (28). Sirt1 protects LECs from oxidative stress by inhibiting the p53 pathway (29).…”

Section: Introductionmentioning

confidence: 99%

The miRNA-34a/Sirt1/p53 pathway in a rat model of lens regeneration

et al. 2022

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Background: There are many molecular factors involved in Wolffian and corneal lens regeneration, but few in lens regeneration by lens epithelial cells (LECs) in mammals. Silent information regulator 1 (Sirt1) has a variety of physiological functions, such as a transport hub, and is involved in pathological conditions.We studied the expression of the microRNA (miRNA)-34a/Sirt1/tumor protein p53 (p53) pathway in a rat model of lens regeneration.Methods: We performed extracapsular lens extraction in 42 healthy female Sprague-Dawley rats. Slit lamp observation was performed at 3, 7, 14, 21, 30, 60 and 90 days postoperatively, and the rats were killed humanely by cervical dislocation at 30, 60 and 90 days postoperatively to remove the eyeballs. We performed semiquantitative immunofluorescence analysis of Sirt1, p53, alpha-smooth muscle actin (α-SMA) and fibronectin (fn), and real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) to detect the relative expressions of miRNA-34a, Sirt1, p53, aquaporin 0 (AQP 0), γA-crystallin, and beaded filament structural protein 1 (BFSP1) mRNA in the lens and posterior capsule. Results:The posterior capsule wrinkled at 3 days and it increased at 7 days. At 14 days, pearl-like opacification appeared under the capsule, with increasing shrinkage. Greater mass-like proliferators in size and number accumulated under the capsule and at the equator after 21 days. A regenerated lens developed in the central depression of the capsule at 30 days, slightly protruding from it. Despite being thickened at 60 days, the central depression persisted, with a smaller change at 90 days than at 60 days. Although the relative mRNA expression of miRNA-34a and p53 in the lens and posterior capsule decreased over time (P=0.000), that of Sirt1 increased (P<0.01). α-SMA was uniformly expressed in the crystals and gradually decreased, while fn expression gradually increased.Conclusions: miRNA-34a expression decreased and Sirt1 expression increased during lens regeneration. Furthermore, p53 expression decreased, thus reducing apoptosis. Therefore, Sirt1 acted as a key factor in the pathway, and played a protective role in lens regeneration.

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Expression of miR‑34a in cataract rats and its related mechanism

Cited by 6 publications

References 21 publications

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

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

Alternate Causes for Pathogenesis of Exfoliation Glaucoma, a Multifactorial Elastotic Disorder: A Literature Review

The miRNA-34a/Sirt1/p53 pathway in a rat model of lens regeneration

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