miR‐200c regulates endothelin‐1 induced PASMCs abnormal proliferation and apoptosis

Yuan, Chao; Xu, Min; Rong, Rong; Mei, Yong; Cai, Wei; Li, Lin; Xue, Yue; Zhu, Baoli; Sun, Kai; Han, Lei

doi:10.1002/iub.1686

Cited by 6 publications

(4 citation statements)

References 36 publications

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“…MicroRNAs have cell-type specific roles (Guduric-Fuchs et al, 2012), and miR-200c is enriched in the brain, particularly in neurons, oligodendrocytes (Buller et al, 2012;Lau et al, 2008) and microglia (Tang et al, 2017;Yu et al, 2015). MiR-200c expression increases in response to oxidative stress (Lee et al, 2010; and suppresses MAP2 expression (Yuan et al, 2017). In the present study utilizing this novel complexing method we confirmed a high degree of co-localization with miR 200c and neurons and low miR-200c in astrocytes.…”

Section: Discussionsupporting

confidence: 77%

Expression of miR-200c corresponds with increased reactive oxygen species and hypoxia markers after transient focal ischemia in mice

Arvola

Griffiths

Rao

et al. 2021

Neurochemistry International

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Section: Discussionsupporting

confidence: 77%

Expression of miR-200c corresponds with increased reactive oxygen species and hypoxia markers after transient focal ischemia in mice

Arvola

Griffiths

Rao

et al. 2021

Neurochemistry International

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“…Additionally, inhibition of miR-93 increased cell viability and suppresses cell apoptosis in glaucoma HTM cells (29). miR-200c and PTEN are both factors involved in regulating cell apoptosis (30,31). The present study demonstrated that the level of PTEN was negatively regulated by miR-200c-3p.…”

Section: Discussionmentioning

confidence: 99%

miR‑200c‑3p regulates the proliferation and apoptosis of human trabecular meshwork cells by targeting PTEN

2020

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Glaucoma is an optic neuropathy that may lead to visual field loss and blindness. Human trabecular meshwork (HTM) cell dysfunction increases intraocular pressure, which leads to glaucoma. microRNAs (miRs) are single-stranded non-coding RNAs that regulate cellular processes in HTM cells. The aim of the present study was to evaluate the role of miR-200c-3p in HTM cells. HTM cells were treated with 300 µM H 2 o 2 , and the expression of miR-200c-3p was measured by reverse transcription-quantitative polymerase chain reaction. The expression of miR-200c-3p was significantly downregulated under oxidative stress. Phosphatase and tensin homolog (PTEN) was predicted to be a potential target of miR-200c-3p using TargetScan, and this was confirmed by a dual-luciferase reporter assay. The expression of PTEN was upregulated in H 2 o 2 -treated HTM cells. In addition, PTEN expression was negatively regulated by miR-200c-3p. Then, cell proliferation and apoptosis were measured by Cell Counting Kit-8 and flow cytometry assays, respectively. The results demonstrated that the overexpression of miR-200c-3p enhanced cell proliferation and inhibited cell apoptosis, while PTEN reversed the effects of miR-200c-3p. In addition, miR-200c-3p suppressed the expression of PTEN, cleaved caspase-3 and Bax, and improved the expression of phosphorylated (p)-AKT, AKT and p-serine/threonine-protein kinase mTOR (mTOR), while PTEN attenuated these effects. Taken together, these data suggested that overexpression of miR-200c-3p targets PTEN to suppress cleaved caspase-3 and Bax expression and activate the PTEN/AKT/mTOR signaling pathway, thereby resulting in the promotion of cell proliferation and the inhibition of cell apoptosis. These results revealed the role of miR-200c-3p in HTM cells and its underlying molecular mechanism, which may provide a potential target for the treatment of patients with glaucoma.

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“…PR‐positive breast cancer cells show a better outcome than PR‐negative, which is probably supported by an increased miR‐30b/c expression (Croset et al, ; Van Asten et al, ). Additionally, in PR‐positive breast cancer, miR‐200c acts as an antioncogene and inhibits cell migration (Yuan et al, ). In line with this, the lifespan of patients with low amounts of miR‐200c is significantly reduced because of the missing impact of miR‐200c on PR expression (Tuomarila et al, 2014; http://targetcan.org).…”

Section: Progesterone and Prsmentioning

confidence: 99%

Progesterone Effects in the Nervous System

Theis

Theiß

2019

The Anatomical Record

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The sex hormone progesterone is mainly known as a key factor in establishing and maintaining pregnancy. In addition, progesterone has been shown to induce morphological changes in the central and peripheral nervous system by increasing dendrito-, spino-, and synaptogenesis in Purkinje cells (Wessel et al.: Cell Mol Life Sci (2014a) 1723-1740 and increasing axonal outgrowth in dorsal root ganglia (Olbrich et al.: Endocrinology (2013) 3784-3795). These effects mediated mainly by the classical progesterone receptors (PRs) A and B seem to be limited to young neurons. It may be assumed that microRNAs (miRNAs), which are potent regulators of nervous system maturation and degeneration, are also involved in the regulation of progesterone-mediated neuronal plasticity by altering the expression patterns of the corresponding PR A/B receptors (Theis and Theiss: Neural Regen Res (2015) 547-549, Pieczora et al.: Cerebellum (2017) 376-387). This review critically discusses current data on the neuroprotective effect of progesterone and its corresponding receptors in the nervous system, with possible regulatory processes by miRNAs. Preclinical studies on stroke and traumatic brain injury revealed neuroprotective and neuroregenerative effects of progesterone in the treatment of severe neurological diseases in animal models, but have so far failed in humans. In this context, the identification of specific miRNAs that regulate the expression of progesterone and PR could help to exploit the neuroprotective potential of progesterone for the treatment of various neurological disorders. The human nervous system is a highly complex tissue composed of neurons and glial cells with a limited ability to regenerate after lesion or degeneration. In particular, the loss of neurons, for example, due to aging processes, stroke, or traumatic brain injury (TBI), is mostly irreversible. The function of the degenerating neurons can be partially compensated by neighboring neurons, but astroglial-fibrotic scar formation minimizes neuronal regeneration .Progesterone, a sexual hormone, is mainly known for its key role in the female reproductive circuit and the maintenance of pregnancy. In this context, the fact that progesterone is also expressed in the male organism is often neglected (Schumacher et al., 2014). Besides this, Abbreviations: BBB = blood brain barrier; CNS = central nervous system; DRG = dorsal root ganglia; GABA = Gamma-amino butyric acid; miRNA = microRNA; NMDAR = N-Methyl-D-aspartate receptor; PC = Purkinje cells; PGRMC1 = progesterone receptor membrane component 1; PNS = peripheral nervous system; PR = progesterone receptor; SCI = spinal cord injury; TBI = traumatic brain injury

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miR‐200c regulates endothelin‐1 induced PASMCs abnormal proliferation and apoptosis

Cited by 6 publications

References 36 publications

Expression of miR-200c corresponds with increased reactive oxygen species and hypoxia markers after transient focal ischemia in mice

Expression of miR-200c corresponds with increased reactive oxygen species and hypoxia markers after transient focal ischemia in mice

miR‑200c‑3p regulates the proliferation and apoptosis of human trabecular meshwork cells by targeting PTEN

Progesterone Effects in the Nervous System

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