MicroRNA-494 improves functional recovery and inhibits apoptosis by modulating PTEN/AKT/mTOR pathway in rats after spinal cord injury

Hui, Zhu; Xie, Rong; Liu, Xiaodong; Shou, Jiajun; Gu, Wentao; Gu, Shaohua; Che, Xiaoming

doi:10.1016/j.biopha.2017.05.143

Cited by 62 publications

(51 citation statements)

References 42 publications

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“…Moreover, previous studies revealed that miR-137 could show the suppressive effect on the inflammatory response and apoptosis after SCI (Gao et al, 2018). Importantly, it is interesting that miR-362-3p could be regulated after SCI, which demonstrated by previous research (Zhu et al, 2017). Notably, in the present study, miR-362-3p was used to explore the effect of it on neuropathic pain following SCI.…”

Section: Discussionsupporting

confidence: 57%

“…In addition, the previous evidence confirmed that miRNAs were also involved in regulating neuronal inflammation (Taras-sishin et al, 2011). Interestingly, , as one of 46 downregulated miRNAs, was indicated in rat with spinal cord after contusion SCI (Zhu et al, 2017). However, the function and molecular mechanism of miR-362-3p involved in neuropathic pain following SCI are still unclear.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Liu

Zhang

et al. 2019

J. Integr. Neurosci.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Liu

Zhang

et al. 2019

J. Integr. Neurosci.

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“…Similarly, the transfection of miR-99b-5p inhibitor could promote neuro-regeneration in SCI mice through the activation of mTOR pathway [1]. By performing miRNA microarray analyses, miR-92a-3p has been found to be obviously down-regulated after SCI surgery [22]. Previous studies have demonstrated that miR-92a-3p is involved in many different types of diseases such as T-cell acute lymphoblastic leukemia [32], renal injury-associated atherosclerosis [33] and colorectal cancer [34].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, miRNAs were used to control the expression of PTEN. Zhu et al [22] demonstrated that miR-494 could directly regulate the expression of PTEN, and up-regulating the level of miR-494 in SCI rats effectively down-regulates the mRNA and protein levels of PTEN and then promotes the activation of AKT/mTOR pathway. Similarly, miR-29a has also been identified to be able to specifically target the 3 -UTR of PTEN mRNA, and overexpressed miR-29a by a recombinant lentiviral vector greatly enhances the phosphorylation of Akt and S6 and promotes the functional recovery of hindlimbs of SCI rats [44].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, the elevation of miR-21 contributes to the repair of injured spinal cords through suppressing programmed cell death 4 (PDCD4) [21]; miR-544a is down-regulated after SCI, and up-regulating miR-544a levels could effectively attenuate inflammation and promote the recovery of spinal cord through inhibiting neurogenic differentiation 4 (NEUROD4) expression [3]. Moreover, miR-92a-3p is found to be significantly down-regulated after SCI [22], however, its functions in SCI pathology remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog

Wang

et al. 2020

Bioscience Reports

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Spinal cord injury (SCI) is a neurological disease commonly caused by traumatic events on spinal cords. MiRNA-92a-3p is reported to be down-regulated after SCI. Our study investigated the effects of up-regulated miR-92a-3p on SCI and the underlying mechanisms. SCI mice model was established to evaluate the functional recovery of hindlimbs of mice through open-field locomotion and scored by Basso, Beattie, and Bresnahan (BBB) locomotion scale. Apoptosis of spinal cord cells was determined by flow cytometry. The effects of miR-92a-3p on SCI were detected by intrathecally injecting miR-92a-3p agomiR (agomiR-92) into the mice prior to the establishment of SCI. Phosphatase and tensin homolog (PTEN) was predicted as a target of miR-29a-3p by TargetScan. We further assessed the effects of agomiR-92 or/and overexpressed PTEN on apoptosis rates and apoptotic protein expressions in SCI mice. Moreover, the activation of protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling was determined by Western blot. The results showed that compared with the sham-operated mice, SCI mice had much lower BBB scores, and theapoptosis rate of spinal cord cells was significantly increased. After SCI, the expression of miR-92a-3p was down-regulated, and increased expression of miR-92a-3p induced by agomiR-92 further significantly increased the BBB score and decreased apoptosis. PTEN was specifically targeted by miR-92a-3p. In addition, the phosphorylation levels of Akt and mTOR were up-regulated under the treatment of agomiR-92. Our data demonstrated that the neuroprotective effects of miR-92a-3p on spinal cord safter SCI were highly associated with the activation of the PTEN/AKT/mTOR pathway.

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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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MicroRNA-494 improves functional recovery and inhibits apoptosis by modulating PTEN/AKT/mTOR pathway in rats after spinal cord injury

Cited by 62 publications

References 42 publications

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog

Progesterone Effects in the Nervous System

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