Jiadifenolide induces the expression of cellular communication network factor (CCN) genes, and CCN2 exhibits neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells

Shoji, Masaki; Ueda, Masako; Nishioka, Motomu; Minato, Hiroki; Seki, Masahide; Harada, Kenichi; Kubo, Miwa; Suzuki, Yutaka; Aoyama, Eriko; Takigawa, Masaharu; Kuzuhara, Takashi

doi:10.1016/j.bbrc.2019.09.003

Cited by 9 publications

(2 citation statements)

References 29 publications

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“…In addition, the CCN2 protein was confirmed to exhibit neurotrophic effects and promote phosphorylation of the p44/42 MAPK protein in human neuronal cells. This result suggests that the molecular mechanism by which 32 exerts its neurotrophic effect is linked with CCN signaling [116]. It should be noted that this is the first discovery to connect neurotrophic effects with CCN signaling.…”

Section: Neurotrophic Compounds From Illicium Speciesmentioning

confidence: 68%

The search for, and chemistry and mechanism of, neurotrophic natural products

Kubo

Harada

2020

J Nat Med

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Neurotrophic factors, now termed neurotrophins, which belong to a class of polypeptidyl agents, have been shown to potentially be beneficial for the treatment of neurodegenerative diseases such as Alzheimer's disease, because endogenous neurotrophic factors (NGF, BDNF, NT3, NT4) have been recognized to play critical roles in the promotion of neurogenesis, differentiation, and neuroprotection throughout the development of the central nervous system. However, high-molecular weight proteins are unable to cross the blood-brain barrier and are easily decomposed by peptidase under physiological conditions. To address this issue, small molecules that can mimic the functions of neurotrophic factors would be promising alternatives for the treatment of neurodegenerative disease. We have continued to search for natural products having typical neurotrophic properties, which can cause neurogenesis, enhance neurite outgrowth, and protect neuronal death using three cellular systems (PC12, rat cortical neurons, and MEB5 cells). In this review, we summarize the neurotrophic activities and synthesis of dimeric isocuparane-type sesquiterpenes from the liverwort, Mastigophora diclados, the mechanism of neurotrophic neolignans, magnolol, honokiol and their sesquiterpene derivatives, and introduce unique neurotrophin-mimic natural products, including seco-prezizaane-type sesquiterpenes from the Illicium species, vibsane-type diterpenes from Viburnum awabuki, and miscellaneous natural products with neurotrophic effects discovered by us.

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Section: Neurotrophic Compounds From Illicium Speciesmentioning

confidence: 68%

The search for, and chemistry and mechanism of, neurotrophic natural products

Kubo

Harada

2020

J Nat Med

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“…The CTGF protein acts as a neurotrophic factor via activation of the p44/42 mitogen-activated protein kinase (MAPK) signaling pathway. 25) Since p44/42 mediates cell proliferation and neurogenesis of neural progenitor cells, 26) increased expression of CTGF may also protect dopaminergic neurons through the promotion of cell proliferation and neurogenesis. These results may indicate that YAP activation by LATS inhibition activates p44/42 via transcriptional upregulation of CTGF, which reduced 6-OHDA-induced dopaminergic nerve damage.…”

Section: Discussionmentioning

confidence: 99%

LATS Inhibitor Protects 6-OHDA Induced Neuronal Cell Death <i>In Vitro</i> and <i>In Vivo</i>

Fujimori,

Ohba,

Nakamura

et al. 2023

BPB Reports

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Parkinson's disease (PD) is a neurodegenerative disorder marked by progressive motor dysfunction. Dopaminergic neurons in the substantia nigra are likely the main cause of PD onset. The Hippo signaling pathway regulates organ size and tumor suppression. The Yes-associated protein (YAP) is a nuclear effector of the Hippo signaling pathway, and activation of YAP may be beneficial in several neurodegenerative diseases. In this study, we examined the effects of compound A [N-(tert-butyl)-2-(pyridin-4-yl)-1,7-naphthyridin-4-amine], a large tumor suppressor kinase (LATS) inhibitor, on 6-hydroxydopamine (6-OHDA)-induced cell damage in vitro and in vivo. In human neuroblastoma SH-SY5Y cells, compound A showed a protective effect against 6-OHDAinduced cell death without exhibiting any cytotoxicity. In order to investigate the effects of compound A on dopaminergic neurons, compound A was orally administrated to mice twice a day for 21 d. Next, mouse brains were harvested to assess the expression of (1) a dopaminergic neuron marker and (2) a YAP transcriptional target. Treatment of mice with 6-OHDA suppressed the expression of tyrosine hydroxylase (TH), a dopaminergic neuron marker, and compound A (3 mg/kg, per os) administration ameliorated the TH expression levels. In addition, compound A upregulated the mRNA expression levels of connective tissue growth factor (CTGF), a YAP transcriptional target. These results suggest that activation of the Hippo signaling pathway by LATS inhibition may be used as a novel therapeutic target for treating PD.

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Enantioselective Construction of 5‐6‐5 Tricyclic Lactone Framework Bearing a Quaternary Bridgehead Carbon via Rh‐Catalyzed Asymmetric [2+2+2] Cycloaddition of Enediynes

et al. 2021

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Herein, we report a Rh-catalyzed asymmetric [2 + 2 + 2] cycloaddition of ene-yne-yne enediynes to generate enantio-enriched tricyclic cyclohexadienes bearing a quaternary bridgehead carbon. We found that the Rh-Phanephos complex is an appropriate catalyst for the cycloaddition of enediynes bearing an unsubstituted propiolate terminus, whereas Rh-biaryl bisphosphine catalysts, which have been widely used for asymmetric cycloadditions of alkynes and alkenes, are not applicable for the reaction of such enediynes. Several control experiments suggest that the reaction using the Rh-Phanephos complex exclusively proceeds via a rhodacyclopentadiene intermediate, unlike when using a Rh-biaryl bisphosphine complex that can form a rhodacyclopentadiene intermediate as well as a rhodacyclopentene intermediate in a substratedependent manner.

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Jiadifenolide induces the expression of cellular communication network factor (CCN) genes, and CCN2 exhibits neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells

Cited by 9 publications

References 29 publications

The search for, and chemistry and mechanism of, neurotrophic natural products

The search for, and chemistry and mechanism of, neurotrophic natural products

LATS Inhibitor Protects 6-OHDA Induced Neuronal Cell Death <i>In Vitro</i> and <i>In Vivo</i>

Enantioselective Construction of 5‐6‐5 Tricyclic Lactone Framework Bearing a Quaternary Bridgehead Carbon via Rh‐Catalyzed Asymmetric [2+2+2] Cycloaddition of Enediynes

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