Cloning and Stable Expression of cDNA Coding For Platelet Endothelial Cell Adhesion Molecule -1 (PECAM-1, CD31) in NIH-3T3 Cell Line

Salehi-Lalemarzi, Hamed; Shanehbandi, Dariush; Shafaghat, Farzaneh; Abbasi-Kenarsari, Hajar; Baradaran, Behzad; Movassaghpour, Aliakbar; Kazemi, Tohid

doi:10.15171/apb.2015.034

Cited by 4 publications

(4 citation statements)

References 25 publications

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“…Mouse embryonic fibroblast NIH3T3 was widely used in cellular signal transduction, protein-protein interaction, and molecular activity assays because it was easy to maintain, transfect, and grow. [22][23][24] In this study, NIH3T3 cells were used to generate transgenic cell lines for stable expression of hRAGE.…”

Section: Introductionmentioning

confidence: 99%

Establishment and Application of Engineered NIH 3T3 Cell Line with Stable Human RAGE Expression

Xiao

Chen

Paerhati

et al. 2020

Pharmaceutical Fronts

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Abstract Aim NIH3T3 cell line with expression of human receptor for advanced glycation end-products (hRAGE) transduced with lentivirus vectors was used to analyze affinity, biological activity, and/or molecular mechanisms of molecules targeting the hRAGE pathway. Method The DNA fragment coding for hRAGE gene was integrated into the genome of NIH3T3 cells using lentivirus transduction. Cells expressing hRAGE were selected with puromycin, and the level of hRAGE expression was analyzed by Western blot. To establish a stable cell line, colonies of hRAGE-expressing cells were generated, and the level of RAGE expression in each engineered cell line was analyzed within 20 generations. Flow cytometry assay was used to verify affinity of anti-hRAGE antibody binding to hRAGE on the surface of engineered cells. The engineered NIH3T3 cell line was applied to assess effects of anti-hRAGE blocking antibody on amyloid β-induced cells apoptosis by CCK-8 assay. Results The engineered NIH3T3 cell line (hRAGE-NIH3T3) could stably express human RAGE. Commercial anti-RAGE polyclonal antibody could recognize and bind to human RAGE on the surface of hRAGE-NIH3T3 but not original NIH3T3 cells. In addition, hRAGE-NIH3T3 was more sensitive to RAGE pathway-dependent stimulation. Our data show that the hRAGE-NIH3T3 cell line established is an excellent tool in the study of RAGE-targeting molecules based on the cellular level, biological function, and RAGE-mediated molecular mechanisms.

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Section: Introductionmentioning

confidence: 99%

Establishment and Application of Engineered NIH 3T3 Cell Line with Stable Human RAGE Expression

Xiao

Chen

Paerhati

et al. 2020

Pharmaceutical Fronts

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“…Complex cellular and molecular processes, including inflammation, cell migration, angiogenesis, temporary matrix synthesis, collagen deposition, and re-epithelialization, characterize normal skin regeneration [7]. There is a complex cascade of events in skin repair, angiogenesis, and angiogenesis, which play a key role in wound healing and are associated with the expression of several cytokines and angiogenic factors [6], [28], [29], [30].…”

Section: Discussionmentioning

confidence: 99%

Topical Polydeoxyribonucleotide Loaded in Hydrogel Formulation for Wound Healing in Diabetic Rats

Dmitriyeva

Suleimenov

Yessenbayev

et al. 2022

Open Access Maced J Med Sci

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Patients with diabetes mellitus experience delayed wound healing because of the uncontrolled glucose level leads to impaired cell proliferative function, poor circulation, decreased production and repair of new blood vessels. Polydeoxyribonucleotide (PDRN) is used in wound healing as a substance that stimulates tissue repair. A hydrogel is a reticular substance generally used as a dressing formulation to accelerate wound healing, and also used as a bio-applicable scaffold or vehicle. The aim of study is to investigate the effects of PDRN loaded in hydrogel on wound healing, in combination and separately, in an animal diabetic wound model. Methods: We studied the effects of PDRN in diabetes-related healing defect using an incisional skin-wound model produced on the back of male diabetic rats. A total of 36 wounds, were classified into 3 groups: a control group, a hydrogel-only group, a PDRN loaded in hydrogel combined-treatment group. All rats were assessed for changes in wound size and photographed on scheduled dates. The skin specimen sample of diabetic rat wound model were observed on 3, 7, 14 and 21 days after skin injury to measure tissue remodeling through histological evaluation of fibroblasts proliferation, and collagen production, also the number of blood vessels was measured in all specimens. Results: Differences in the decrease and change in wound size in the PDRN loaded in hydrogel group were more significant than those in the control and hydrogel single-treatment groups. Analysis of the fibroblasts proliferation, collagen production and number of blood vessels through histological examination showed a pattern of increase over time that occurred in PDRN loaded in hydrogel combined-treatment group. Conclusion: This experiment demonstrated improved wound healing using a PDRN loaded in hydrogel combined treatment compared to either two groups, resulting in a decrease in diabetic wound size and a shortening of the healing period

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“…In particular, TNF-α is a proalgesic cytokine that is abundantly secreted following tissue injury, which not only promotes inflammation but also contributes to pain hypersensitivity in nociceptors ( Hall et al, 2016 ). PECAM1 plays crucial roles in angiogenesis, integration and maintenance of the cytoskeleton and release of leukocytes in the inflammatory sites ( Salehi-Lalemarzi et al, 2015 ). Though angiogenesis promotes embryonic development and is critical for several biological processes during adulthood, it may induce or augment several pathological conditions including inflammation ( Sajib et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

PECAM1 Combines With CXCR4 to Trigger Inflammatory Cell Infiltration and Pulpitis Progression Through Activating the NF-κB Signaling Pathway

Yong-hong

Zhang

et al. 2020

Front. Cell Dev. Biol.

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Pulpitis is a frequent bacterially driven inflammation featured with the local accumulation of inflammatory products in human dental pulps. A GEO dataset GSE16134 comprising data of inflamed dental pulp tissues was used for bioinformatics analyses. A protein-protein interaction (PPI) analysis suggested that chemokine receptor 4 (CXCR4) owned a high correlation with platelet endothelial cell adhesion molecule-1 (PECAM1). A rat model with pulpitis was established, and lipopolysaccharide (LPS)-induced human dental pulp fibroblasts (HDPFs) were used for in vitro experiments. Then, high expression of PECAM1 and CXCR4 was validated in the inflamed dental pulp tissues in rats and in LPS-induced HDPFs. Either downregulation of PECAM1 or CXCR4 suppressed inflammatory cell infiltration in inflamed tissues as well as the inflammation and apoptosis of HDPFs. A transcription factor myocyte-enhancer factor 2 (MEF2C) was predicted and validated as a positive regulator of either PECAM1 or CXCR4, which activated the NF-κB signaling pathway and promoted pulpitis progression. To sum up, this study suggested that MEF2C transcriptionally activates PECAM1 and CXCR4 to activate the B-cell and NF-κB signaling pathways, leading to inflammatory cell infiltration and pulpitis progression.

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Cloning and Stable Expression of cDNA Coding For Platelet Endothelial Cell Adhesion Molecule -1 (PECAM-1, CD31) in NIH-3T3 Cell Line

Cited by 4 publications

References 25 publications

Establishment and Application of Engineered NIH 3T3 Cell Line with Stable Human RAGE Expression

Establishment and Application of Engineered NIH 3T3 Cell Line with Stable Human RAGE Expression

Topical Polydeoxyribonucleotide Loaded in Hydrogel Formulation for Wound Healing in Diabetic Rats

PECAM1 Combines With CXCR4 to Trigger Inflammatory Cell Infiltration and Pulpitis Progression Through Activating the NF-κB Signaling Pathway

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