Aβ induces PUMA activation: a new mechanism for Aβ-mediated neuronal apoptosis

Feng, Jie; Meng, Chengbo; Xing, Da

doi:10.1016/j.neurobiolaging.2014.10.007

Cited by 21 publications

(11 citation statements)

References 61 publications

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“…The cerebral ECs are the main components that support the essential functions of the BBB. Several studies show that Aβ can induce neuronal or ECs apoptosis through caspase‐dependent pathway in a time‐ and dose‐dependent manner (Feng, Meng, & Xing, ; Fossati, Ghiso, & Rostagno, ). The caspases is a family of cysteine proteases and critical mediators of programmed cell death.…”

Section: Discussionmentioning

confidence: 99%

Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Liu

Kang

et al. 2018

Phytotherapy Research

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Excessive amyloid beta (Aβ) deposition in brain is mainly responsible for cell damage and blood-brain barrier (BBB) disruption in Alzheimer's disease (AD). Catalpol, an iridoid glucoside extracted from the root of Rehmannia glutinosa Libosch, has neuroprotective effect against AD. It is unclear whether catalpol has a protective effect on Aβ-induced BBB leakage. We employed an immortalized endothelial cell line (bEnd.3) and astrocytes co-culture to mimic a BBB model in vitro and investigated the effect of catalpol on BBB. We found that treatment with catalpol decreased BBB hyperpermeability induced by fibrillar Aβ . Data from western blotting showed that catalpol prevented fibrillar Aβ -induced bEnd.3 cell apoptosis through mitochondria-dependent and death receptor pathways; decreased the levels of matrix metalloproteinases (MMPs), MMP-2, MMP-9, and the receptor for advanced glycation end products; and increased the levels of tight junction proteins (ZO-1, occludin, and claudin-5), low-density lipoprotein receptor-related protein 1, and P-glycoprotein in fibrillar Aβ -treated bEnd.3 cells. Moreover, catalpol also enhanced soluble Aβ efflux across the fibrillar Aβ -treated bEnd.3 cells BBB monolayer model. Altogether, our results suggest that catalpol alleviate fibrillar Aβ -induced BBB disruption, enhance soluble Aβ clearance, and offer a feasible therapeutic application in AD treatment.

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Section: Discussionmentioning

confidence: 99%

Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Liu

Kang

et al. 2018

Phytotherapy Research

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“…P53 upregulated modulator of apoptosis (PUMA), which has a powerful pro-apoptotic effect, is a key protein in apoptosis and might be a potential new target for radio-gene therapy (13)(14)(15). It has been reported that PUMA could increase sensitivity to radiation-induced apoptosis in certain kinds of tumor cells both in vivo and in vitro (15)(16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Slug inhibition increases radiosensitivity of oral squamous cell carcinoma cells by upregulating PUMA

Jiang

Zhou

Wei

et al. 2016

International Journal of Oncology

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As a new strategy, radio-gene therapy was widely used for the treatment of cancer patients in recent few years. Slug was involved in the radioresistance of various cancers and has been found to have an anti-apoptotic effect. This study aims to investigate whether the modulation of Slug expression by siRNA affects oral squamous cell carcinoma sensitivity to X-ray irradiation through upregulating PUMA. Two oral squamous cell carcinoma cell lines (HSC3 and HSC6) were transfected with small interfering RNA (siRNA) targeting Slug and subjected to radiotherapy in vitro. After transfection with Slug siRNA, both HSC3 and HSC6 cells showed relatively lower expression of Slug and higher expression of PUMA. The Slug siRNA transfected cells showed decreased survival and proliferation rates, an increased apoptosis rate and enhanced radiosensitivity to X-ray irradiation. Our results revealed that Slug siRNA transfection in combination with radiation increased the expression of PUMA, which contributed to radiosensitivity of oral squamous cell carcinoma cells. Thus, controlling the expression of Slug might contribute to enhance sensitivity of HSC3 and HSC6 cells toward X-ray irradiation in vitro by upregulating PUMA.

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“…It is widely accepted that neuronal apoptosis is pathological feature of AD . Aβ42 is considered as one of the main causes of neuronal apoptosis . The mushroom body represents the main sensory integrative center of an insect's brain and plays a major role in memory.…”

Section: Resultsmentioning

confidence: 99%

Imidazole improves cognition and balances Alzheimer's‐like intracellular calcium homeostasis in transgenic Drosophila model

Zhang

Wang

et al. 2017

Neurourology and Urodynamics

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Aβ induces PUMA activation: a new mechanism for Aβ-mediated neuronal apoptosis

Cited by 21 publications

References 61 publications

Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Slug inhibition increases radiosensitivity of oral squamous cell carcinoma cells by upregulating PUMA

Imidazole improves cognition and balances Alzheimer's‐like intracellular calcium homeostasis in transgenic Drosophila model

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Aβ induces PUMA activation: a new mechanism for Aβ-mediated neuronal apoptosis

Cited by 21 publications

References 61 publications

Catalpol provides a protective effect on fibrillary Aβ1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Catalpol provides a protective effect on fibrillary Aβ1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Slug inhibition increases radiosensitivity of oral squamous cell carcinoma cells by upregulating PUMA

Imidazole improves cognition and balances Alzheimer's‐like intracellular calcium homeostasis in transgenic Drosophila model

Contact Info

Product

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Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Catalpol provides a protective effect on fibrillary Aβ_1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier