Publications by authors named "L N Ma"

17,045 Publications

MicroRNA-383-5p regulates osteogenic differentiation of human periodontal ligament stem cells by targeting histone deacetylase 9.

Authors:
Lan Ma Di Wu

Arch Oral Biol 2021 May 25;129:105166. Epub 2021 May 25.

Department of Stomatology, Jingmen No.1 People's Hospital, China. Electronic address:

Objective: Human periodontal ligament stem cells (hPDLSCs) play an important role in regenerative engineering technology for periodontal therapy. The mechanism of microRNA (miR)-383-5p in osteogenic differentiation needs further exploration. This study aimed at investigating the potential role of miR-383-5p in the osteogenic differentiation of hPDLSCs.

Methods: Osteogenic differentiation of hPDLSCs was induced by osteoblastinducing media and evaluated by Alizarin Red staining and Alkaline phosphatase staining. To examine the role of miR-383-5p in osteogenic differentiation, miR-383-5p mimic or inhibitor and histone deacetylase (HDAC) 9 overexpression plasmid or siRNA-HDAC9 were co-transfected into hPDLSCs. qRT-PCR and Western blot were applied for detection of mRNA and protein levels.

Results: During the osteogenic differentiation of hPDLSCs, miR-383-5p expression was gradually up-regulated, while HDAC9 mRNA level was down-regulated. HDAC9 overexpression suppressed Alkaline phosphatase activity, mineral node formation and the expressions of osteogenic markers including Runx family transcription factor 2 (RUNX2), osteocalcin and Smad family member 4 (Smad4) in the differentiated hPDLSCs, while siHDAC9 exerted opposite effects on osteogenic differentiation. The Alkaline phosphatase activity, mineral node formation and the expressions of RUNX2, osteocalcin and Smad4 of the differentiated hPDLSCs were regulated by miR-383-5p/HDAC9 axis. The miR-383-5p/HDAC9 axis effectively regulated the expressions of osteogenic markers during the differentiation of hPDLSCs.

Conclusion: MiR-383-5p overexpression facilitated the osteogenic differentiation of hPDLSCs via inhibiting HDAC9 expression.
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http://dx.doi.org/10.1016/j.archoralbio.2021.105166DOI Listing
May 2021

MiR-124 protects against cognitive dysfunction induced by sevoflurane anesthesia in vivo and in vitro through targeting calpain small subunit 1 via NF-κB signaling pathway.

Adv Clin Exp Med 2021 Jun 11. Epub 2021 Jun 11.

Department of Anesthesiology, The Third Hospital of Hebei Medical University, Shijiazhuang, China.

Background: Postoperative cognitive dysfunction (POCD) is an impairment of cognition that affects post-surgery patients. Sevoflurane anesthesia is linked to cognitive dysfunction correlated to the expression of miRNA levels.

Objectives: In the current study, we investigated if miR-124 can offer protection against cognitive deficits induced by sevoflurane in a spatial learning paradigm, and examined the molecular mechanisms through cell cultures.

Material And Methods: Escape latency, platform crossings in probe trials and swimming speed in the Morris water maze in sevoflurane-treated mice were utilized as a measure of cognitive function. The relative miR-124 expression, and mRNA expressions of Bax, caspase-3 and Bcl-2 in sevoflurane-treated hippocampal cultures were measured using real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the changes in interleukin (IL)-1β, tumor necrosis factor alpha (TNF-α) and IL-6 were determined using enzyme-linked immunosorbent assay (ELISA). The binding between miR-124 and calpain small subunit 1 (Capn4) was verified with site-directed mutagenesis. The involvement of the nuclear factor kappa B (NF-κB) signaling pathway was examined using western blot analysis.

Results: Our findings indicated that the miR-124 expression was inhibited by sevoflurane treatment in live rats and mouse hippocampal neurons to prevent apoptosis and inflammatory responses. We confirmed Capn4 as a target of miR-124. Treatment with sevoflurane enhanced the expression of Capn4, while overexpression of miR124 suppressed the enhanced expression of Capn4. Also, miR-124 inhibited apoptosis in murine hippocampal neurons induced by sevoflurane via the NF-κB signaling pathway.

Conclusions: Our findings demonstrated that miR-124 exerted its neuroprotective role against sevoflurane via targeting Capn4 and NF-κB signaling pathways. Our work may provide a novel and efficacious treatment for sevoflurane anesthesia-related cognitive dysfunction.
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http://dx.doi.org/10.17219/acem/134740DOI Listing
June 2021

VE-cadherin N-glycosylation modified by GnT-V regulates VE-cadherin/β-catenin interaction and monocyte adhesion.

Exp Physiol 2021 Jun 12. Epub 2021 Jun 12.

College of Pharmacy, Chongqing Medical University, Chongqing, 400016, P.R. China.

New Findings: What is the central question of this study? Inflammation-induced monocyte adhesion is the initiator of most vascular diseases. The underlying mechanisms mediating monocyte adhesion remain to be fully clarified. What is the main finding and its importance? GnT-V medicated N-glycosylation on VE-cadherin regulates the dissociation of VE-cadherin/β-catenin complex to modulate the monocyte adhesion, but GnT-V overexpression can not rescue monocyte adhesion induced by IL-1β. This study enriched the molecular mechanism of VE-cadherin in regulating the monocyte adhesion process.

Abstract: Monocyte adhesion is a critical step in the initial stage of atherosclerosis, and dysfunction of VE-cadherin was reported to be involved in this process. Our group has found that VE-cadherin and its binding protein, β-catenin, were modified by sialylation, and the sialylation levels were both decreased in proinflammatory cytokine-treated EA.hy926 cells. In this study, we further confirmed the sugar chains of on VE-cadherin were modified by GnT-V. Results showed that the levels of GnT-V and β1,6 GlcNAc on the VE-cadherin were decreased in the presence of IL-1β, while the level of monocyte transendothelial migration was increased. Moreover, the interaction between VE-cadherin and β-catenin was increased, accompanied by an increased accumulation of degradative VE-cadherin and cytoplasmic β-catenin, indicating the impairment of cell-cell junction after IL-1β treatment. Furthermore, GnT-V shRNA and overexpression analysis confirmed that glycosylation of VE-cadherin was modified by GnT-V in EA. hy926 cells, which contributed to the monocyte-endothelial adhesion process. Taken together, these results suggested that the function of VE-cadherin in facilitating monocyte adhesion might result from the decreasing GnT-V expression and GnT-V-catalyzed N-glycosylation disorder. Our study enriched the molecular mechanism of VE-cadherin in regulating the monocyte adhesion process, and opened new insights into the post-transcriptional modifications on VE-cadherin. This article is protected by copyright. All rights reserved.
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http://dx.doi.org/10.1113/EP089617DOI Listing
June 2021

Genetic dissection of maize seedling traits in an IBM Syn10 DH population under the combined stress of lead and cadmium.

Mol Genet Genomics 2021 Jun 11. Epub 2021 Jun 11.

Key Laboratory of Biology and Genetic Improvement of Maize in Southwest Region, Maize Research Institute, Sichuan Agricultural University, Chengdu, 611130, China.

The heavy metals lead and cadmium have become important pollutants in the environment, which exert negative effects on plant morphology, growth and photosynthesis. It is particularly significant to uncover the genetic loci and the causal genes for lead and cadmium tolerance in plants. This study used an IBM Syn10 DH population to identify the quantitative trait loci (QTL) controlling maize seedling tolerance to lead and cadmium by linkage mapping. The broad-sense heritability of these seedling traits ranged from 65.8-97.3% and 32.0-98.8% under control (CK) and treatment (T) conditions, respectively. A total of 53 and 64 QTL were detected under CK and T conditions, respectively. Moreover, 42 QTL were identified using lead and cadmium tolerance coefficient (LCTC). Among these QTL, five and two major QTL that explained > 10% of phenotypic variation were identified under T condition and using LCTC, respectively. Furthermore, eight QTL were simultaneously identified by T and LCTC, explaining 5.23% to 9.21% of the phenotypic variations. Within these major and common QTL responsible for the combined heavy metal tolerance, four candidate genes (Zm00001d048759, Zm00001d004689, Zm00001d004843, Zm00001d033527) were previously reported to correlate with heavy metal transport and tolerance. These findings will contribute to functional gene identification and molecular marker-assisted breeding for improving heavy metal tolerance in maize.
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http://dx.doi.org/10.1007/s00438-021-01800-2DOI Listing
June 2021

Rapid determination of viable but non-culturable Campylobacter jejuni in food products by loop-mediated isothermal amplification coupling propidium monoazide treatment.

Int J Food Microbiol 2021 Jun 1;351:109263. Epub 2021 Jun 1.

Food Nutrition and Health Program, Faculty of Land and Food Systems, The University of British Columbia, Vancouver, BC V6T 1Z4, Canada; Department of Food Science and Agricultural Chemistry, Faculty of Agricultural and Environmental Sciences, McGill University, Ste Anne de Bellevue, QC H9X 3V9, Canada. Electronic address:

Campylobacter is the leading cause of foodborne human diarrhea worldwide. This microbe in the viable but non-culturable (VBNC) state can evade detection by routinely used culture-based methods and remain viable for extended periods of time. Bacteria in this dormancy state can resume their metabolic activity and virulence by resuscitation under favorable conditions, and subsequently cause infections. In this study, an assay combining loop-mediated isothermal amplification (LAMP) and propidium monoazide (PMA) treatment was developed for the detection and quantification of VBNC C. jejuni in agri-foods. PMA-qLAMP targeting the hipO gene demonstrated 100% high specificity to C. jejuni. A linear detection of C. jejuni was achieved between 8.77 × 10 and 8.77 × 0 CFU/mL with a coefficient of determination (R) of 0.9956, indicating a good quantitative capacity. C. jejuni was effectively induced into the VBNC state by osmotic stress (i.e., 7% NaCl, w/v) over 48 h. VBNC C. jejuni cells were spiked into three representative food products and determined by PMA-qLAMP coupled with plating assay. The detection limits of PMA-qLAMP were 1.58 × 10 CFU/mL in milk, 3.78 × 10 CFU/g in chicken breast meat, and 4.33 × 10 CFU/g in romaine lettuce. PMA-qLAMP demonstrated rapid (25-40 min), specific (100% inclusivity and 100% exclusivity) and sensitive (~10 CFU/mL) determination of VBNC C. jejuni. This method can be applied in the agri-food industry to decrease the risks related to the consumption of contaminated agri-foods with pathogenic bacteria in the VBNC state and reduce the burden of C. jejuni infections to public health.
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http://dx.doi.org/10.1016/j.ijfoodmicro.2021.109263DOI Listing
June 2021