ClC-2 knockdown prevents cerebrovascular remodeling via inhibition of the Wnt/ β-catenin signaling pathway.

Conclusion: This study demonstrates that blocking ClC-2-mediated Cl- efflux inhibits AngII-induced cerebrovascular smooth muscle cell proliferation and migration by inhibiting the Wnt/β-catenin pathway. Our data indicate that downregulation of ClC-2 may be a viable strategy in the prevention of hyperplasia and remodeling of cerebrovascular smooth muscle cells. PMID: 29988306 [PubMed - in process]
Source: Cellular and Molecular Biology Letters - Category: Biochemistry Authors: Tags: Cell Mol Biol Lett Source Type: research

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In conclusion, LAZ3 protects against cardiac remodeling in DCM by decreasing miR-21, thus regulating PPARa/NRF2 signaling.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research
In conclusion, the cardioprotection of TMP against LPS-induced injury was through up-regulating the expression of 14-3-3γ, promoting the translocation of Bcl-2 to mitochondria, and improving the function of mitochondria. PMID: 29782860 [PubMed - as supplied by publisher]
Source: European Journal of Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Eur J Pharmacol Source Type: research
Background: Late exercise preconditioning (LEP) is confirmed to have a protective effect on acute cardiovascular stress. However, the mechanisms by which mitophagy participates in exercise preconditioning (EP)-induced cardioprotection remain unclear. LEP may involve mitophagy mediated by the receptors PARK2 gene–encoded E3 ubiquitin ligase (Parkin) and BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (Bnip3) to scavenge damaged mitochondria. Methods: Our EP protocol involved four 10-minute periods of running, separated by 10-minute recovery intervals, plus a period of exhaustive running at 24 hours after...
Source: Journal of Cardiovascular Pharmacology - Category: Cardiology Tags: Original Article Source Type: research
Authors: Schorch B, Heni H, Zahaf NI, Brummer T, Mione M, Schmidt G, Papatheodorou P, Aktories K Abstract Clostridium perfringens toxin TpeL belongs to the family of large clostridial glycosylating toxins. The toxin causes N-acetylglucosaminylation of Ras proteins at threonine35 thereby inactivating the small GTPases. Here, we show that all main types of oncogenic Ras proteins (H-Ras, K-Ras and N-Ras) are modified by the toxin in vitro and in vivo. Toxin-catalyzed modification of Ras was accompanied by inhibition of the MAP kinase pathway. Importantly, TpeL inhibited the paradoxical activation of the MAP kinase pat...
Source: Oncotarget - Category: Cancer & Oncology Tags: Oncotarget Source Type: research
Abstract Alpha lipoic acid (α-LA), a potent antioxidant, is protective against acute nephrotoxicity. In the present study, the attenuation of cadmium (Cd)-induced kidney injury by α-LA on was investigated in a rat model. Exposure to 50 mg/L Cd for 12 weeks increased kidney index and Cd content, malondialdehyde (MDA) levels, and histological damage to the renal cortex, and decreased the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Treatment with 50 mg/L Cd also damaged renal cell mitochondria and nuclei, and activated the mitocho...
Source: Journal of Inorganic Biochemistry - Category: Biochemistry Authors: Tags: J Inorg Biochem Source Type: research
In this study, the Ad-GFP-HO-1C[INCREMENT]23 group showed better kinematic functional recovery after SCI than the Ad-GFP and Vehicle groups, as well as smaller reductions in TJ proteins and capillary permeability compared with those in the Ad-GFP and Vehicle groups. These findings indicated that Ad-GFP-HO-1C[INCREMENT]23 might have a potential therapeutic effect that is mediated by its protection of BSCB integrity.
Source: NeuroReport - Category: Neurology Tags: Clinical Neuroscience Source Type: research
Conclusion: Our study revealed that mDia1 plays a critical role in AGE-induced microvascular hyperpermeability through binding to RAGE.Cell Physiol Biochem 2018;45:1717 –1730
Source: Cellular Physiology and Biochemistry - Category: Cytology Source Type: research
Conclusions: In summary, our data demonstrate that TFEB is a positive regulator of angiogenesis through activation of AMPKα and autophagy, suggesting that TFEB constitutes a novel molecular target for ischemic vascular disease. PMID: 29467198 [PubMed - as supplied by publisher]
Source: Circulation Research - Category: Cardiology Authors: Tags: Circ Res Source Type: research
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Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: Original Article Source Type: research
Publication date: 5 April 2018 Source:Journal of Hazardous Materials, Volume 347 Author(s): Juan Zhuang, Shan Wang, Qun Shan, Zi-feng Zhang, Meng-qiu Li, Gui-hong Zheng, Shao-hua Fan, Dong-mei Wu, Bin Hu, Jun Lu, Yuan-lin Zheng Evidence indicates that oxidative stress is the central pathological feature of 2, 2´, 4, 4´-tetrabromodiphenyl ether (BDE-47)-induced neurotoxicity. Protein kinase C delta (PKCδ), an oxidative stress-sensitive kinase, can be proteolytically cleaved to yield a catalytically active fragment (PKCδ-CF) that is involved in various neurodegenerative disorders. Here, we showed tha...
Source: Journal of Hazardous Materials - Category: Environmental Health Source Type: research
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