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1.
Med Sci Monit ; 28: e936542, 2022 03 03.
Artículo en Inglés | MEDLINE | ID: mdl-35236816

RESUMEN

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Yun-Qian Wang, Cong-Cong Fan, Bao-Ping Chen, Jun Shi. Resistin-Like Molecule Beta (RELM-ß) Regulates Proliferation of Human Diabetic Nephropathy Mesangial Cells via Mitogen-Activated Protein Kinases (MAPK) Signaling Pathway. Med Sci Monit 2017; 23:3897-3903. DOI: 10.12659/MSM.905381.

2.
Med Sci Monit ; 23: 3897-3903, 2017 08 12.
Artículo en Inglés | MEDLINE | ID: mdl-28801998

RESUMEN

BACKGROUND Resistin-like molecule beta (RELM-ß) has been reported to be associated with diabetic nephropathy (DN). However, the role of RELM-ß in DN is poorly understood. This study was conducted to delineate the underlying mechanisms of action and to investigate the role of RELM-ß in the primitive development of DN via MAPK signaling pathways. MATERIAL AND METHODS Lentivirus-mediated vectors and RNAi technology were used to establish the model of RELM-ß up-regulated and down-regulated expression in human mesangial cells (HMCs). The proliferation of HMCs was detected through CCK-8 method. The cell cycle and cell proliferation of HMCs was detected through flow cytometry. The MAPKs pathway protein activity was detected through Western blotting. RESULTS The HMCs with up-regulated and down-regulated expression of RELM-ß increased or decreased significantly at 2-3 days. The HMCs with high glucose intervention reversed the proliferation inhibition. The HMCs with exogenous glucose or RELM-ß protein intervention partially reversed the cell cycle inhibition. Among the MAPKs pathway, the phosphorylation activity of p38MAPK and JNK increased or decreased and ERK1/2 did not change in the overexpression or inhibition of RELM-ß. The p38 MAPK pathway inhibitor SB202190 significantly inhibited the proliferation of HMCs caused by overexpression of RELM-ß. Up-regulated expression of RELM-b induced the phosphorylation of p38 MAPK, JNK in HMCs and promoted HMCs proliferation and participated in early DN through the MAPKs pathway. CONCLUSIONS The results provide evidence that RELM-b is a potential molecular target for the treatment of DN.


Asunto(s)
Nefropatías Diabéticas/metabolismo , Péptidos y Proteínas de Señalización Intercelular/metabolismo , Sistema de Señalización de MAP Quinasas , Ciclo Celular/fisiología , División Celular/fisiología , Proliferación Celular/fisiología , Células Cultivadas , Nefropatías Diabéticas/patología , Humanos , Células Mesangiales/metabolismo , Células Mesangiales/patología , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Fosforilación , Factor de Crecimiento Transformador beta1/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo
3.
Dalton Trans ; 45(27): 10909-15, 2016 Jul 05.
Artículo en Inglés | MEDLINE | ID: mdl-27301344

RESUMEN

An anionic zeolite-like metal-organic framework (AZMOF) with a twisted partially augmented the net, known as the "Moravia" net, [(CH3)2NH2]6[Sr13(O)3()8(OH)2(H2O)16]·xS (, where S represents non-coordinated solvent molecules, and is the abbreviation of benzo-(1,2;3,4;5,6)-tris-(thiophene-2'-carboxylic acid)), has been solvothermally synthesized and characterized, which possesses an anionic framework and nano-sized sodalite cage. Through cation-exchange, is capable of uptaking large organic cationic dyes including Rhodamine B (RB), Basic Red 2 (BR2), Crystal Violet (CV) and Methylene Blue (MB), amongst which the adsorption capability for RB (up to 545 mg g(-1)), and BR2 (up to 675 mg g(-1)) is the highest for reported absorbants to date.

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