Axin-2 knockdown promote mitochondrial biogenesis and dopaminergic neurogenesis by regulating Wnt/β-catenin signaling in rat model of Parkinson's disease

Singh, Sonu; Mishra, Akanksha; Mohanbhai, Soni Jignesh; Tiwari, Virendra; Chaturvedi, Rajnish Kumar; Khurana, Sukant; Shukla, Shubha

doi:10.1016/j.freeradbiomed.2018.08.033

Cited by 57 publications

(42 citation statements)

References 91 publications

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“…Corroborating our earlier findings, a number of recent studies have highlighted the critical importance of WβC crosstalk with survival and inflammatory pathways in inciting neurogenesis and neurorepair Kalamakis et al, 2019;Kase, Otsu, Shimazaki, & Okano, 2019;Mishra et al, 2019;Morrow & Moore, 2019;Ray et al, 2018;Singh, Mishra, Bharti, et al, 2018b;Singh, Mishra, Mohanbhai, et al, 2018a;Singh, Mishra, & Shukla, 2016).…”

Section: Introductionsupporting

confidence: 85%

“…Here, activation of WβC-signalling using the specific GSK-3β inhibitor SB216763 efficiently counteracted the 6-OHDA-induced neurogenic impairment at both the SVZ and SGZ levels. In the hippocampus, GSK-3β inhibition enhanced dendritic arborization and survival of granular neurons and stimulated NSC differentiation towards the neuronal phenotype in the DG(Singh et al, 2018b;Singh, Mishra, Mohanbhai, et al, 2018a).Together, these in vivo findings suggested a disruption of WβCsignalling associated with decreased proliferation and neuroblast formation in the MPTP-injured SVZ, and further documented the ability of pharmacological activation of β-catenin-mediated signalling to counteract the impaired neurogenic potential of MPTP or Dkk1-infused mice. Coupled to the recent findings obtained at the SGZ level, these data highlight WβC as a key pathway for the regulation of NSC homeostasis during basal ganglia injury induced by the neurotoxins MPTP and 6-OHDA, both in the SVZ-and hippocampal SGZ-niches.…”

mentioning

confidence: 63%

“…This inhibitory effect was efficiently counteracted by concomitant activation of the downstream transcriptional effector, β-catenin, with systemic AR injections (Figure S2). Very recently, the beneficial effect of WβC activation was reported(Singh, Mishra, Bharti, et al, 2018b;Singh, Mishra, Mohanbhai, et al, 2018a) in the 6-OHDA rat model of PD. Here, activation of WβC-signalling using the specific GSK-3β inhibitor SB216763 efficiently counteracted the 6-OHDA-induced neurogenic impairment at both the SVZ and SGZ levels.…”

mentioning

confidence: 99%

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Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

et al. 2020

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A common hallmark of age‐dependent neurodegenerative diseases is an impairment of adult neurogenesis. Wingless‐type mouse mammary tumor virus integration site (Wnt)/β‐catenin (WβC) signalling is a vital pathway for dopaminergic (DAergic) neurogenesis and an essential signalling system during embryonic development and aging, the most critical risk factor for Parkinson's disease (PD). To date, there is no known cause or cure for PD. Here we focus on the potential to reawaken the impaired neurogenic niches to rejuvenate and repair the aged PD brain. Specifically, we highlight WβC‐signalling in the plasticity of the subventricular zone (SVZ), the largest germinal region in the mature brain innervated by nigrostriatal DAergic terminals, and the mesencephalic aqueduct‐periventricular region (Aq‐PVR) Wnt‐sensitive niche, which is in proximity to the SNpc and harbors neural stem progenitor cells (NSCs) with DAergic potential. The hallmark of the WβC pathway is the cytosolic accumulation of β‐catenin, which enters the nucleus and associates with T cell factor/lymphoid enhancer binding factor (TCF/LEF) transcription factors, leading to the transcription of Wnt target genes. Here, we underscore the dynamic interplay between DAergic innervation and astroglial‐derived factors regulating WβC‐dependent transcription of key genes orchestrating NSC proliferation, survival, migration and differentiation. Aging, inflammation and oxidative stress synergize with neurotoxin exposure in “turning off” the WβC neurogenic switch via down‐regulation of the nuclear factor erythroid‐2‐related factor 2/Wnt‐regulated signalosome, a key player in the maintenance of antioxidant self‐defense mechanisms and NSC homeostasis. Harnessing WβC‐signalling in the aged PD brain can thus restore neurogenesis, rejuvenate the microenvironment, and promote neurorescue and regeneration.

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Section: Introductionsupporting

confidence: 85%

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confidence: 63%

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confidence: 99%

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Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

et al. 2020

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“…In the absence of the ligand, β-catenin is phosphorylated by GSK3β in a cytoplasmic complex containing auxin, APC (the adenomatous polyposis coli protein), and β-catenin [84]. Then, the phosphorylated β-catenin is ubiquitinated and degraded into the proteasome [85]. In the presence of VacA, GSK3β is inactivated and leads to the accumulation of β-catenin in the cytoplasm [86].…”

Section: Vacuolating Cytotoxin a And Gastric Cancermentioning

confidence: 99%

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Alipour

2020

J Gastrointest Canc

153

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Introduction Various types of cancers threaten human life. The role of bacteria in causing cancer is controversial, but it has been determined that the Helicobacter pylori infection is one of the identified risk factors for gastric cancer. Helicobacter pylori infection is highly prevalent, and about half of the world , s population is infected with it. Objective The aim of this study was the role of Helicobacter pylori in the development of gastric cancer. Method We obtained information from previously published articles. Results and Conclusion The bacterium has various virulence factors, including cytotoxin-associated gene A, vacuolating cytotoxin A, and the different outer membrane proteins that cause cancer by different mechanisms. These virulence factors activate cell signaling pathways such as PI3-kinase/Akt, JAK/STAT and Ras, Raf, and ERK signaling that control cell proliferation. Uncontrolled proliferation can lead to cancer.

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“…Mitochondrial dysfunction occurs in patients with COPD, and this includes abnormal mitochondrial biogenesis, fusion/fission, and mitophagy (Mizumura et al, 2014;Ahmad et al, 2015). Wnt signaling has been shown to regulate mitochondrial biogenesis and fusion/fission, which is cell-and organ-specific (An et al, 2010;Yoon et al, 2010;Godoy et al, 2014;Bernkopf and Behrens, 2018;Singh et al, 2018). For instance, activation of Wnt signal by Wnt3a results in an increase in mitochondria in human osteosarcoma cell.…”

Section: Wnt Pathway In Copdmentioning

confidence: 99%

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Gao

et al. 2019

J Pharmacol Exp Ther

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Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with progressive airflow limitation and functional decline. The pathogenic mechanisms for this disease include oxidative stress, inflammatory responses, disturbed protease/antiprotease equilibrium, apoptosis/proliferation imbalance, senescence, autophagy, metabolic reprogramming, and mitochondrial dysfunction. The Wnt signaling pathway is an evolutionarily conserved signaling pathway that is abnormal in COPD, including chronic bronchitis and pulmonary emphysema. Furthermore, Wnt signaling has been shown to modulate aforementioned cellular processes involved in COPD. From this perspective, we provide an updated understanding of the crosstalk between Wnt signal and these cellular processes, and highlight the crucial role of the Wnt signal during the development of COPD. We also discuss the potential for targeting the Wnt signal in future translational and pharmacological therapeutics aimed at prevention and treatment of this disease.

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Axin-2 knockdown promote mitochondrial biogenesis and dopaminergic neurogenesis by regulating Wnt/β-catenin signaling in rat model of Parkinson's disease

Cited by 57 publications

References 91 publications

Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

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