THE RELATIONSHIP BETWEEN THE EXPRESSION LEVELS OF TISSUE INHIBITOR OF METALLOPROTEINASES-3 (TIMP3) AND SEVERITY OF ATHEROSCLEROSIS

Background: MicroRNAs (miRNA) are known to play a key role in the etiology and treatment of epilepsy through controlling the expression of gene. However, miR-125a-5p in the epilepsy is little known. Epilepsy in rat models was induced by Pentylenetetrazol (PTZ) and miR- 125a-5p profiles in the hippocampus were investigated in our experiment. Also, the relationship between miR-125a-5p and calmodulin-dependent protein kinase IV (CAMK4) was identified and the related mechanism was also illustrated. Methods: The miR-125a-5p mRNA expression levels were evaluated by quantitative real time polymerase chain reaction (qRT-PCR). Western Blot (WB) was used to analyze the CAMK4 protein expression levels. Seizure score, latency and duration were determined based on a Racine scale. The enzyme-linked immunosorbent assay (ELISA) was used to analyze the inflammatory factor expression. The relationship between miR-125a-5p and CAMK4 was detected through dual luciferase assay. Results: Downregulation of miR-125a-5p was observed in the hippocampus of PTZ-induced epilepsy rats. The overexpression of miR-125a-5p attenuated seizure and decreased inflammatory factor level in the hippocampus of PTZ-induced rats. The miR-125a-5p alleviated epileptic seizure and inflammation in PTZ-induced rats by suppressing its target gene, CAMK4. Conclusion: miR-125a-5p may represent a novel therapeutic treatment for PTZ-induced epilepsy by preventing the activation of CAMK4.

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Insights into the Role of Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases in Health and Disease

Current Chemical Biology ◽

10.2174/221279680803150420095017 ◽

2015 ◽

Vol 8 (3) ◽

pp. 184-214

Author(s):

Sudip Das ◽

Sreejani Bandopadhyay ◽

Swati Das

Keyword(s):

Matrix Metalloproteinases ◽

Tissue Inhibitor Of Metalloproteinases ◽

Tissue Inhibitor ◽

Health And Disease

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High Resolution Structure of the N-terminal Domain of Tissue Inhibitor of Metalloproteinases-2 and Characterization of Its Interaction Site with Matrix Metalloproteinase-3

Journal of Biological Chemistry ◽

10.1074/jbc.273.34.21736 ◽

1998 ◽

Vol 273 (34) ◽

pp. 21736-21743 ◽

Cited By ~ 65

Author(s):

Frederick W. Muskett ◽

Tom A. Frenkiel ◽

James Feeney ◽

Robert B. Freedman ◽

Mark D. Carr ◽

...

Keyword(s):

High Resolution ◽

Matrix Metalloproteinase ◽

Tissue Inhibitor Of Metalloproteinases ◽

Tissue Inhibitor ◽

Interaction Site ◽

Matrix Metalloproteinase 3 ◽

Terminal Domain ◽

High Resolution Structure ◽

Resolution Structure

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Decitabine shows anti-acute myeloid leukemia potential via regulating the miR-212-5p/CCNT2 axis

Open Life Sciences ◽

10.1515/biol-2020-0097 ◽

2020 ◽

Vol 15 (1) ◽

pp. 1013-1023

Author(s):

Lina Xing ◽

Jinhai Ren ◽

Xiaonan Guo ◽

Shukai Qiao ◽

Tian Tian

Keyword(s):

Acute Myeloid Leukemia ◽

Cell Viability ◽

Cell Apoptosis ◽

Myeloid Leukemia ◽

Luciferase Reporter ◽

Expression Levels ◽

Proliferation And Apoptosis ◽

Polymerase Chain ◽

The Relationship ◽

Acute Myeloid

AbstractPrevious research has revealed the involvement of microRNA-212-5p (miR-212-5p) and cyclin T2 (CCNT2) in acute myeloid leukemia (AML). However, whether the miR-212-5p/CCNT2 axis is required for the function of decitabine in AML has not been well elucidated. Quantitative reverse transcription-polymerase chain reaction was used to examine enrichment of miR-212-5p. The relationship between CCNT2 and miR-212-5p was verified by the luciferase reporter assay. Cell apoptosis was evaluated by flow cytometry and western blot. CCK-8 assay was performed to determine cell viability. Decitabine significantly repressed cell viability, while promoted cell apoptosis. Meanwhile, the expression levels of cyclinD1, CDK4, and Bcl-2 were suppressed in cells with decitabine exposure, but Bax and caspase-3 expression levels were upregulated. Besides, miR-212-5p upregulation had the similar function with decitabine in AML cell proliferation and apoptosis. Subsequently, restoration of CCNT2 attenuated miR-212-5p overexpression-induced effects in Kasumi-1 and SKNO-1 cells. In addition, miR-212-5p depletion reversed decitabine-induced CCNT2 downregulation. The miR-212-5p/CCNT2 axis had an implication in the anti-leukemic effect of decitabine in AML.

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