Chronic Intermittent Ethanol Exposure Induces Upregulation of Matrix Metalloproteinase-9 in the Rat Medial Prefrontal Cortex and Hippocampus

Yin, Litian; Li, Fengqing; Li, Jue; Yang, Xiaorong; Xie, Xiaoyan; Xue, Linyuan; Li, Yanli; Zhang, Ce

doi:10.1007/s11064-019-02783-8

Cited by 10 publications

(9 citation statements)

References 46 publications

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“…Recent studies suggest that matrix metalloproteinase-9 (MMP-9), a Zn ( 2 ) + dependent extracellular endopeptidase, participates in neuronal plasticity, specifically in memory and learning ( 161 , 162 ). Acute and chronic ethanol exposure up-regulates the MMP-9 levels in the brain, particularly in the medial pre-frontal cortex and hippocampus, in rats ( 163 ). The vascular endothelial growth factor (VEGF) is involved in the activity, plasticity and survival of microvessels.…”

Section: Developmental Stages Of the Fetal Brainmentioning

confidence: 99%

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

et al. 2020

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Prenatal alcohol exposure is associated to different physical, behavioral, cognitive, and neurological impairments collectively known as fetal alcohol spectrum disorder. The underlying mechanisms of ethanol toxicity are not completely understood. Experimental studies during human pregnancy to identify new diagnostic biomarkers are difficult to carry out beyond genetic or epigenetic analyses in biological matrices. Therefore, animal models are a useful tool to study the teratogenic effects of alcohol on the central nervous system and analyze the benefits of promising therapies. Animal models of alcohol spectrum disorder allow the analysis of key variables such as amount, timing and frequency of ethanol consumption to describe the harmful effects of prenatal alcohol exposure. In this review, we aim to synthetize neurodevelopmental disabilities in rodent fetal alcohol spectrum disorder phenotypes, considering facial dysmorphology and fetal growth restriction. We examine the different neurodevelopmental stages based on the most consistently implicated epigenetic mechanisms, cell types and molecular pathways, and assess the advantages and disadvantages of murine models in the study of fetal alcohol spectrum disorder, the different routes of alcohol administration, and alcohol consumption patterns applied to rodents. Finally, we analyze a wide range of phenotypic features to identify fetal alcohol spectrum disorder phenotypes in murine models, exploring facial dysmorphology, neurodevelopmental deficits, and growth restriction, as well as the methodologies used to evaluate behavioral and anatomical alterations produced by prenatal alcohol exposure in rodents.

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Section: Developmental Stages Of the Fetal Brainmentioning

confidence: 99%

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

et al. 2020

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“…Thus, the miR-29b-3p/MMP-9 axis was investigated in subsequent assays. In a recent study, integrin β1 and α-tubulin were identified as potential MMP-9-interacting proteins ( 25 ). To examine the interaction between MMP-9 and integrin β1/α-tubulin, Myc-integrin β1/Myc-α-tubulin and HA-MMP-9 were transiently co-expressed in 293T cells and Co-IP assays were performed using a HA antibody.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have shown that the hemopexin domain of MMP-9 can interact with different integrin subunits to promote enhanced cancer cell migration, invasion and proliferation in various cancer cell types, such as colon cancer cells, B cell chronic lymphocytic leukemia and breast cancer cells (39)(40)(41)(42). Notably, the integrin β1, Src, elongation factor 1-α 2, α-tubulin, actin and histone H2B proteins are potential MMP-9-interacting proteins (25). In the present study, it was shown that integrin β1 and MMP-9 bind directly (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…These studies suggested that MMP-9 binds to integrin proteins to regulate α-tubulin acetylation and deacetylation, and is involved in regulating polyp formation. Of note, a recent study showed that integrin β1 and α-tubulin proteins were potential MMP-9-interacting proteins ( 25 ). Thus, the present study aimed to pursue these ideas further.…”

Section: Introductionmentioning

confidence: 99%

“…Lee et al ( 23 ) found that MMP-9 and integrin β1 activity can increase α-tubulin acetylation. Of note, Smith ( 24 ) and Yin et al ( 25 ) found that integrin β1 is a potential MMP-9-interacting protein. Thus, we hypothesized that downregulation of miR-29b-3p promotes α-tubulin acetylation by increasing MMP-9 binding to integrin β1, and the present study aimed to provide novel insight into the etiology and pathogenesis of CRSwNPs.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of miR‑29b‑3p promotes α‑tubulin deacetylation by targeting the interaction of matrix metalloproteinase‑9 with integrin β1 in nasal polyps

Liu

et al. 2021

Int J Mol Med

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Matrix metalloproteinase (MMP)-9 is a key enzyme responsible for extracellular matrix degradation and contributes to the progressive histological changes observed in lower respiratory tract infections. Integrin β1 and α-tubulin are potential MMP-9-interacting proteins, and microRNA (miR)-29b-3p can regulate MMP-9 expression. MMP-9 is highly expressed in chronic rhinosinusitis with nasal polyps (cRSwNPs), regardless of its effects on miR-29b-3p, integrin β1 and α-tubulin expression. In the present study, samples from 100 patients with cRSwNPs were examined via reverse transcription-quantitative PcR to assess the mRNA expression of miR-29b-3p, and western blotting was performed to assess the protein expression of MMP-2, MMP-9, acetyl-α-tubulin, integrin β1 and tissue inhibitor of metalloproteinase 1 (TIMP-1). A dual-luciferase reporter assay was used to verify the direct binding of miR-29b-3p and MMP-2/MMP-9. co-immunoprecipitation (co-IP) and GST pull-down assays showed that integrin β1 and α-tubulin were MMP-9-interacting proteins. Cell viability, apoptosis and inflammatory cytokine levels were determined via a Cell Counting Kit-8 assay, flow cytometry and ELISA, respectively. miR-29b-3p expression was found to be positively correlated with MMP-2 and MMP-9 expression. Whereas, TIMP-1 expression was negatively correlated with MMP-2 and MMP-9 expression. The dual-luciferase assay revealed that miR-29b-3p targeted the 3' untranslated region of MMP-2/MMP-9. The co-IP and GST pull-down assays showed that MMP-9 could directly bind to integrin β1 and indirectly bind to α-tubulin. Finally, the overexpression of miR-29b-3p decreased the expression of MMP-9 and increased the levels of acetyl-α-tubulin. By contrast, the knockdown of miR-29b-3p increased the expression of MMP-9 and decreased the levels of acetyl-α-tubulin. Additionally, MMP-9 expression was found to be negatively correlated with acetyl-α-tubulin expression. Of note, the expression of integrin β1 did not change following the overexpression and knockdown of MMP-9. Finally, the overexpression of miR-29b-3p not only decreased MMP-9 expression, but also alleviated lipopolysaccharide-induced inflammation in NP69 cells. The results showed that the downregulation of miR-29b-3p promoted α-tubulin deacetylation by increasing the number of MMP-9-integrin β1 complexes in cRSwNPs, thus targeting miR-29b-3p/MMP-9 may be a potential novel strategy for the clinical treatment of cRSwNPs.

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