Browsing by Author "Anuradha Yadav"

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Correction to: Inhibitory Effects of Bisphenol-A on Neural Stem Cells Proliferation and Differentiation in the Rat Brain Are Dependent on Wnt/β-Catenin Pathway (Molecular Neurobiology, (2015), 52, 3, (1735-1757), 10.1007/s12035-014-8940-1)
(Humana Press Inc., 2019) Shashi Kant Tiwari; Swati Agarwal; Brashket Seth; Anuradha Yadav; Ratan Singh Ray; Vijay Nath Mishra; Rajnish Kumar Chaturvedi
The original version of this article unfortunately contained a mistake. The authors observed inadvertent error in Figure 3A and 6C wish to correct it. The corrected representative images are incorporated below. This correction in no way changes the text of the article, conclusion and figure legend. The authors regret for this error and would like to apologize for any inconvenience caused to the readers. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Inhibitory Effects of Bisphenol-A on Neural Stem Cells Proliferation and Differentiation in the Rat Brain Are Dependent on Wnt/β-Catenin Pathway
(Humana Press Inc., 2015) Shashi Kant Tiwari; Swati Agarwal; Brashket Seth; Anuradha Yadav; Ratan Singh Ray; Vijay Nath Mishra; Rajnish Kumar Chaturvedi
Neurogenesis, a process of generation of new neurons, occurs throughout the life in the hippocampus and sub-ventricular zone (SVZ). Bisphenol-A (BPA), an endocrine disrupter used as surface coating for packaged food cans, injures the developing and adult brain. However, the effects of BPA on neurogenesis and underlying cellular and molecular mechanism(s) are still unknown. Herein, we studied the effect(s) of prenatal and early postnatal exposure of low dose BPA on Wnt/β-catenin signaling pathway that controls different steps of neurogenesis such as neural stem cell (NSC) proliferation and neuronal differentiation. Pregnant rats were treated with 4, 40, and 400 μg BPA/kg body weight orally daily from gestational day 6 to postnatal day 21. Both in vivo and in vitro studies showed that BPA alters NSC proliferation and differentiation. BPA impaired NSC proliferation (5′-bromo-2′-deoxyuridine (BrdU+) and nestin+ cells) and neuronal differentiation (BrdU/doublecortin+ and BrdU/neuronal nuclei (NeuN+) cells) in the hippocampus and SVZ as compared to control. It significantly altered expression/protein levels of neurogenic genes and the Wnt pathway genes in the hippocampus. BPA reduced cellular β-catenin and p-GSK-3β levels and decreased β-catenin nuclear translocation, and cyclin-D1 and TCF/LEF promoter luciferase activity. Specific activation and blockage of the Wnt pathway suggested involvement of this pathway in BPA-mediated inhibition of neurogenesis. Further, blockage of GSK-3β activity by SB415286 and GSK-3β small interfering RNA (siRNA) attenuated BPA-induced downregulation of neurogenesis. Overall, these results suggest significant inhibitory effects of BPA on NSC proliferation and differentiation in the rat via the Wnt/β-catenin signaling pathway. © 2014, Springer Science+Business Media New York.
Pharmacological Insights: Mitochondrial ROS Generation by FNC (Azvudine) in Dalton’s Lymphoma Cells Revealed by Super Resolution Imaging
(Springer, 2024) Naveen Kumar; Vikram Delu; Ilya Ulasov; Sanjay Kumar; Rishi Kant Singh; Sandeep Kumar; Alok Shukla; Anand Kumar Patel; Lokesh Yadav; Ruchi Tiwari; Kumari Rachana; Shivashish Priyadarshi Mohanta; Varsha Singh; Anuradha Yadav; Kaushalendra Kaushalendra; Arbind Acharya
Nucleoside analogs are a common form of chemotherapy that disrupts DNA replication and repair, leading to cell cycle arrest and apoptosis. Reactive oxygen species (ROS) production is a significant mechanism through which these drugs exert their anticancer effects. This study investigated a new nucleoside analog called FNC or Azvudine, and its impact on ROS production and cell viability in Dalton’s lymphoma (DL) cells. The study found that FNC treatment resulted in a time- and dose-dependent increase in ROS levels in DL cells. After 15 and 30 min of treatment with 2 and 1 mg/ml of FNC, mitochondrial ROS production was observed in DL cells. Furthermore, prolonged exposure to FNC caused structural alterations and DNA damage in DL cells. The results suggest that FNC’s ability to impair DL cell viability may be due to its induction of ROS production and indicate a need for further investigation. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.