The inhibition of miR-17-5p promotes cortical neuron neurite growth via STAT3/GAP-43 pathway

Zhang, Liang; Wang, Zhijie; Li, Bo; Xia, Ziwei; Wang, Xin; Xiu, Yucai; Zhang, Zheng; Chen, Chuanjie; Song, Hong; Li, Wenhua; Yu, Mei; Zhang, Meiling; Wang, Kai; Guo, Xiaoling; Ren, Liqun; Wang, Tianyi

doi:10.1007/s11033-020-05273-1

Cited by 19 publications

(7 citation statements)

References 45 publications

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“…The phosphorylation of JNK subsequently induced activation of Stat1 and Stat3 that led to expressions of βIII-tubulin and GAP-43, and ultimately promoted the differentiation of ES cell neurons [ 72 ]. MiR-17-5p inhibitor promoted the expression of Stat3 and p-Stat3, and then boosted the expression of GAP-43, finally promoted axon growth of the cortical neuron [ 73 ]. Akt2, EF1α and potentially β-tubulin may form part of a signaling complex targeted to sites of cell activity via association with the cytoskeleton and as such may be important in the regulation of cell motility and growth [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Pim-1 Protects Retinal Ganglion Cells by Enhancing Their Regenerative Ability Following Optic Nerve Crush

Zhang

Wang

et al. 2020

Exp Neurobiol

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Provirus integration site Moloney murine leukemia virus (Pim-1) is a proto-oncogene reported to be associated with cell proliferation, differentiation and survival. This study was to explore the neuroprotective role of Pim-1 in a rat model subjected to optic nerve crush (ONC), and discuss its related molecules in improving the intrinsic regeneration ability of retinal ganglion cells (RGCs). Immunofluorescence staining showed that AAV2-Pim-1 infected 71% RGCs and some amacrine cells in the retina. Real-time PCR and Western blotting showed that retina infection with AAV2-Pim-1 up-regulated the Pim-1 mRNA and protein expressions compared with AAV2-GFP group. Hematoxylin-Eosin (HE) staining, γ-synuclein immunohistochemistry, Cholera toxin B (CTB) tracing and TUNEL showed that RGCs transduction with AAV2-Pim-1 prior to ONC promoted the survival of damaged RGCs and decreased cell apoptosis. RITC anterograde labeling showed that Pim-1 overexpression increased axon regeneration and promoted the recovery of visual function by pupillary light reflex and flash visual evoked potential. Western blotting showed that Pim-1 overexpression up-regulated the expression of Stat3, p-Stat3, Akt1, p-Akt1, Akt2 and p-Akt2, as well as βIII-tubulin, GAP-43 and 4E-BP1, and downregulated the expression of SOCS1 and SOCS3, Cleaved caspase 3, Bad and Bax. These results demonstrate that Pim-1 exerted a neuroprotective effect by promoting nerve regeneration and functional recovery of RGCs. In addition, it enhanced the intrinsic regeneration capacity of RGCs after ONC by activating Stat3, Akt1 and Akt2 pathways, and inhibiting the mitochondrial apoptosis pathways. These findings suggest that Pim-1 may prove to be a potential therapeutic target for the clinical treatment of optic nerve injury.

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Section: Discussionmentioning

confidence: 99%

Pim-1 Protects Retinal Ganglion Cells by Enhancing Their Regenerative Ability Following Optic Nerve Crush

Zhang

Wang

et al. 2020

Exp Neurobiol

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“…They were then incubated with primary antibodies against YB-1 and BCRP overnight and subsequently with specific secondary antibodies at room temperature overnight. The results were observed using a fluorescence microscope [ 10 ].…”

Section: Methodsmentioning

confidence: 99%

YB-1 Expression Is Associated with Lymph Node Metastasis and Drug Resistance to Adriamycin in Breast Cancer

Dong

Jian

et al. 2023

Disease Markers

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Background. Breast cancer (BC) is the most common malignant tumor among females. Although there are multiple treatments for breast cancer, many patients still face the dilemma of drug resistance after multiline treatment. It would be greatly helpful for clinical work to identify additional and improved prognostic predictors. Y-box binding protein-1 (YB-1) is a member of the cold shock protein family, and patients with overexpression of YB-1 have a worse prognosis. Methods. This study collected 48 specimens from 48 patients with breast cancer and analyzed the clinicopathological characteristics of the patients. Immunohistochemistry, immunofluorescence, cell viability analysis, tumor spheroid formation and cell morphology, cell invasion, cycle analysis, qRT-PCR, Western blot, and tumorigenicity in BALB/c nude mice were performed to verify the results. Results. We found that patients with overexpression of YB-1 were related to lymph node metastasis and the patients’ age tended to be young. Because of the short follow-up time, a survival analysis could not be performed. Based on the results of in vitro and in vivo experiments, this study indicated that breast cancer cells with overexpression of YB-1 had stronger proliferation, migration, and invasion abilities than cells with low expression of YB-1. Compared with cells with low expression of YB-1, the proliferation, migration, and invasion abilities of YB-1 overexpressed cells were not significantly affected by adriamycin. Conclusion. This suggested that breast cancer cells with overexpression of YB-1 were resistant to adriamycin. Therefore, YB-1 is associated with lymph node metastasis of breast cancer cell. YB-1 could be a prognostic, predictive factor and a novel therapeutic target of BC.

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“…A common receptor component of the IL-6 family is gp130 and after binding cytokines, the JAK/STAT pathway is activated [107]. The major effectors of the JAK/STAT pathway, STAT1 and 3, make a heterodimer or a homodimer and are translocated into the nucleus followed by regulating gene expression of GAP43 [110], Bcl-xL/Bcl-2 [111], and survivin [112] (Figure 4). Deletion of both PTEN and SOCS3 promotes more axonal regeneration after optic nerve injury than a single deletion of PTEN or SOCS3 [113].…”

Section: Intrinsic Survival and Regenerative Pathways For Optic Nerve Regenerationmentioning

confidence: 99%

The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina

Oshitari

2021

IJMS

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Diabetic retinopathy is a major retinal disease and a leading cause of blindness in the world. Diabetic retinopathy is a neurovascular disease that is associated with disturbances of the interdependent relationship of cells composed of the neurovascular units, i.e., neurons, glial cells, and vascular cells. An impairment of these neurovascular units causes both neuronal and vascular abnormalities in diabetic retinopathy. More specifically, neuronal abnormalities including neuronal cell death and axon degeneration are irreversible changes that are directly related to the vision reduction in diabetic patients. Thus, establishment of neuroprotective and regenerative therapies for diabetic neuropathy in the retina is an emergent task for preventing the blindness of patients with diabetic retinopathy. This review focuses on the pathogenesis of the neuronal abnormalities in diabetic retina including glial abnormalities, neuronal cell death, and axon degeneration. The possible molecular cell death pathways and intrinsic survival and regenerative pathways are also described. In addition, therapeutic approaches for diabetic neuropathy in the retina both in vitro and in vivo are presented. This review should be helpful for providing clues to overcome the barriers for establishing neuroprotection and regeneration of diabetic neuropathy in the retina.

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The inhibition of miR-17-5p promotes cortical neuron neurite growth via STAT3/GAP-43 pathway

Cited by 19 publications

References 45 publications

Pim-1 Protects Retinal Ganglion Cells by Enhancing Their Regenerative Ability Following Optic Nerve Crush

Pim-1 Protects Retinal Ganglion Cells by Enhancing Their Regenerative Ability Following Optic Nerve Crush

YB-1 Expression Is Associated with Lymph Node Metastasis and Drug Resistance to Adriamycin in Breast Cancer

The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina

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