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Results for “MIGRATION”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 415 records · Page 23
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

1,25(OH)2D3 attenuates TGF-β1/β2-induced increased migration and invasion via inhibiting epithelial–mesenchymal transition in colon cancer cells

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) has been reported to inhibit proliferation and migration of multiple types of cancer cells. However, the mechanism underlying its anti-metastasis effect is not fully illustrated. In this study, the effect of 1,25(OH)2D3 on TGF-β1/β2-induced epithelial–mesenchymal transition (EMT) is tested in colon cancer cells. The results suggest that 1,25(OH)2D3 inhibited TGF-β1/β2-induced increased invasion and migration of in SW-480 and HT-29 cells. 1,25(OH)2D3 also inhibited the cadherin switch in SW-480 and HT-29 cells. TGF-β1/β2-induced increased expression of EMT-related transcription factors was also inhibited by 1,25(OH)2D3. 1,25(OH)2D3 also inhibited the secretion of MMP-2 and MMP-9 and increased expression of F-actin induced by TGF-β1/β2 in SW-480 cells. Taken together, this study suggests that the suppression of EMT might be one of the mechanisms underlying the anti-metastasis effect of 1,25(OH)2D3 in colon cancer cells. - Highlights: • TGF-β1/β2-induced model of EMT was used in this study to test the effect of 1,25(OH)2D3 on EMT in colon cancer cells. • 1,25(OH)2D3 inhibited TGF-β1/β2-induced increased migration and invasion. • 1,25(OH)2D3 inhibited TGF-β1/β2-induced increased level of EMT-related transcription factors. • 1,25(OH)2D3 inhibited TGF-β1/β2-induced increased expression of F-actin in SW-480 cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

miR-625 suppresses cell proliferation and migration by targeting HMGA1 in breast cancer

Dysregulation of microRNA contributes to the high incidence and mortality of breast cancer. Here, we show that miR-625 was frequently down-regulated in breast cancer. Decrease of miR-625 was closely associated with estrogen receptor (P = 0.004), human epidermal growth factor receptor 2 (P = 0.003) and clinical stage (P = 0.001). Kaplan–Meier and multivariate analyses indicated miR-625 as an independent factor for unfavorable prognosis (hazard ratio = 2.654, 95% confident interval: 1.300–5.382, P = 0.007). Re-expression of miR-625 impeded, whereas knockdown of miR-625 enhanced cell viabilities and migration abilities in breast cancer cells. HMGA1 was confirmed as a direct target of miR-625. The expressions of HMGA1 mRNA and protein were induced by miR-625 mimics, but reduced by miR-625 inhibitor. Re-introduction of HMGA1 in cells expressing miR-625 distinctly abrogated miR-625-mediated inhibition of cell growth. Taken together, our data demonstrate that miR-625 suppresses cell proliferation and migration by targeting HMGA1 and suggest miR-625 as a promising prognostic biomarker and a potential therapeutic target for breast cancer. - Highlights: • miR-625 expression was significantly decreased in breast cancer. • Decrease of miR-625 was associated with poor clinical outcomes and unfavorable overall survival. • miR-625 overexpression inhibits cell proliferation and migration in vitro. • miR-625 directly targets and suppresses the expression of HMGA1.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Daphnetin inhibits invasion and migration of LM8 murine osteosarcoma cells by decreasing RhoA and Cdc42 expression

Daphnetin, 7,8-dihydroxycoumarin, present in main constituents of Daphne odora var. marginatai, has multiple pharmacological activities including anti-proliferative effects in cancer cells. In this study, using a Transwell system, we showed that daphnetin inhibited invasion and migration of highly metastatic murine osteosarcoma LM8 cells in a dose-dependent manner. Following treatment by daphnetin, cells that penetrated the Transwell membrane were rounder than non-treated cells. Immunofluorescence analysis revealed that daphnetin decreased the numbers of intracellular stress fibers and filopodia. Moreover, daphnetin treatment dramatically decreased the expression levels of RhoA and Cdc42. In summary, the dihydroxycoumarin derivative daphnetin inhibits the invasion and migration of LM8 cells, and therefore represents a promising agent for use against metastatic cancer. - Highlights: • Daphnetin, a coumarin-derivative, inhibited invasion and migration of LM8 cells. • Stress fibers and filopodia were decreased by daphnetin treatment. • Daphnetin decreased RhoA and Cdc42 protein expression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Upregulated expression of Nogo-A and NgR in an experimental model of focal microgyria regulates the migration, proliferation and self-renewal of subventricular zone neural progenitors

Nogo-A and its receptor (NgR) were first described as myelin-associated inhibitors of neuronal regeneration in response to injury. In recent years, knowledge about the important role of the Nogo-A protein in several neuronal pathologies has grown considerably. Here, we employed a neonatal cortex freeze-lesion (NFL) model in neonatal rats and measured the expression of Nogo-A and NgR in the resulting cerebrocortical microdysgenesis 5–75 days after freezing injury. We observed marked upregulation of Nogo-A and NgR in protein levels. Furthermore, the migration of neural precursor cells (NPCs) derived from the subventricular zone (SVZ) toward the sits of injury was perturbed by treatment of NgR antagonist peptide NEP1-40. In vitro analysis showed that the knockdown of NgR by lentivirus-delivered siRNA promoted in axonal regeneration and SVZ-derived neural stem cell/progenitor cell (SVZ-NPCs) adhesion and migration, findings which were similar to the effects of NEP1-40. Taken together, our results indicate an important role for NgR in regulating the physiological processes of SVZ-NPCs. The observation of upregulated Nogo-A/NgR in lesion sites in the NFL model suggest that the effects of the perturbed Nogo-A are a key feature during the development and/or the progression of cortical malformation. - Highlights: • NFL model is an accurate experimental reproduction of focal microgyria of FCD. • The increase of the Nogo-A Levels occurs in response to freeze-induced focal lesioning. • Nogo-A/NgR may play a critical role for in the pathologic progression of FCD. • Nogo-A is associated with the migration, proliferation and self-renewal of SVZ-NPCs.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

MAGE-A1 promotes melanoma proliferation and migration through C-JUN activation

MAGE-A1 belongs to the chromosome X-clustered genes of cancer-testis antigen family and is normally expressed in the human germ line but is also overexpressed in various tumors. Previous studies of MAGE-A1 in melanoma mainly focused on methylation changes or its role in immunotherapy, however, its biological functions in melanoma have remained unknown. In order to determine the role of MAGE-A1 in melanoma growth and metastasis, we manipulated melanoma cell lines with overexpression and knockdown of MAGE-A1. Integration of cell proliferation assays, transwell migration and invasion assays, and RNA-Seq analysis revealed that up-regulation of MAGE-A1 dramatically promoted proliferation, migration, and invasion of human melanoma cell lines in vitro, while down-regulation of MAGE-A1 inhibited those characteristics associated with tumor cells. Furthermore, transcriptome sequencing revealed that MAGE-A1 exerts its tumor promoting activity by activating p-C-JUN directly or through ERK-MAPK signaling pathways. Based on our findings, we propose that MAGE-A1 may be a potential therapeutic target for melanoma patients. - Highlights: • MAGE-A1 promotes proliferation and clone formation in melanoma cell lines. • MAGE-A1 enhances tumor cell migration and invasion in melanoma cell lines. • Network including C-JUN, IL8, and ARHGAP29 play critical role in malignant melanoma. • Oncogenic MAGE-A1 increases p-C-JUN levels, possibly via ERK-MAPK signaling pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line

Accumulating evidence has suggested that microRNA-31-5p (miR-31-5p) is dysfunctional in hepatocellular carcinoma (HCC). However, the molecular mechanism of HCC remains unclear. In this study, we investigated the role of miR-31-5p in tumor formation and development of HCC. The expression of miR-31-5p was detected in HCC tissues, corresponding adjacent tissues, normal liver tissues, and HCC cell lines. miR-31-5p mimics and an inhibitor were transfected into HepG2 cells to assess the effects of miR-31-5p on cell proliferation, apoptosis, cell cycle, migration, and invasion assays. Western blotting was used to detect the expression of Sp1 transcription factor (SP1), cyclin D1, and survivin in transfected HCC cells and control cells. The expression of miR-31-5p was significantly decreased in HCC cells and HCC tissues. Overexpression of miR-31-5p inhibited HCC cell growth, migration, and invasion. Overexpression of miR-31-5p reduced the expression of SP1 and cyclin D1, and knockdown of SP1 decreased cyclin D1 expression. The dual luciferase assay showed that miR-31-5p directly targeted SP1 in HepG2. Together, the results suggested that miR-31-5p acted as a tumor suppressor to regulate SP1, and that miR-31-5p could be used as a therapeutic target for the treatment of HCC. - Highlights: • The expression of miR-31-5p was significantly up-regulated in HCC tissues. • Increased expression of miR-31-5p inhibits cell proliferation, migration, and invasion. • Sp1 transcription factor is the target gene for miR-31-5p.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Down-regulation of lncRNA MEG3 promotes hypoxia-induced human pulmonary artery smooth muscle cell proliferation and migration via repressing PTEN by sponging miR-21

Highlights: • Hypoxia induced cell proliferation and migration in PASMCs. • MEG3 expression was down-regulated in PASMCs hypoxia cell models. • MEG3 exerts its role via miR-21/PTEN axis in PASMCs hypoxia cell models. Hypoxia-induced pulmonary hypertension is a life-threatening disease arising from a progressive increase in pulmonary vascular resistance, irreversible pulmonary vascular remodeling and resulting in right ventricular failure. Recent studies suggested that pulmonary artery smooth muscle cell proliferation and migration played an important role in the pathogenesis of hypoxia-induced pulmonary hypertension. However, the mechanisms of hypoxia-induced pulmonary hypertension are complicated and largely unclear. In this study, we discovered that lncRNA MEG3 was down-regulated in human pulmonary artery smooth muscle cell in hypoxia, and inhibition of MEG3 promoted the cell proliferation and cell migration in both normal and hypoxia condition. Further study demonstrated that MEG3 exerted its function via regulation of miR-21 expression in both normal and hypoxia condition. In addition, we displayed the modulation of PTEN by miR-21 and their role in hypoxia. Ultimately, our study illustrated that MEG3 exerts its role via miR-21/PTEN axis in human pulmonary artery smooth muscle cell under both normal and hypoxia conditions.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Effects of connective tissue growth factor (CTGF/CCN2) on condylar chondrocyte proliferation, migration, maturation, differentiation and signalling pathway

Highlights: • It is the first discovery of CCN2 expression in the whole layers of condylar cartilage. • CCN2 promotes condylar chondrocyte migration, maturation and differentiation. • Blocking PI3K/Akt pathway impairs the stimulatory effect of CCN2 on the proliferation of condylar chondrocyte. CCN2, also known as connective tissue growth factor (CTGF), is a 38 kDa cysteine-rich extracellular matrix protein that regulates a sequence of cellular functions and participates in multiple complex biological processes, such as chondrogenesis and osteogenesis. In the present study, we provided the first evidence describing the physiological role of CCN2 in condylar chondrocyte proliferation, migration, maturation and differentiation. CCN2 was widely expressed throughout the whole layers of condylar cartilage and predominantly distributed in the proliferative zone. Recombinant CCN2 promoted the proliferation, migration, proteoglycan synthesis and differentiation capacity of isolated condylar chondrocytes. The stimulatory effect of CCN2 on chondrocyte proliferation was associated with the activation of phosphatidylinositol 3-kinase/Akt signalling pathway. The blocking of this pathway by its inhibitor LY294002 impaired the proliferative effect of CCN2 on chondrocytes. These results suggested a novel physiological role of CCN2 in the development of condylar cartilage.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration

Highlights: • Exocyst Sec10 decreases by I/R injury and restores with functional recovery. • Sec10 inversely regulates kidney tubule cell wound healing after scratch injury. • Sec10 inversely regulates ruffle formation at the leading edge during recovery. • Upregulation of Sec10 increases DGKγ expression at the leading edge during recovery. • DGK inhibitor reversed Sec10-mediated ruffle formation and wound healing defect. Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis

Highlights: • LncRNA XIST was significantly down-regulated in breast cancer. • LncRNA XIST depressed the growth, migration and invasion of breast cancer. • MiR-155 was a direct target of XIST. • LncRNA XIST exerted its function via miR-155/CDX1 axis. Long non-coding RNA (lncRNA) is an important member of non-coding RNA family and emerging evidence has indicated that it plays a pivotal role in many physiological and pathological processes. The lncRNA X inactive specific transcript (XIST) is a potential tumour suppressor in some types of cancers. However, the expression and function of XIST in breast cancer remain largely unclear. The objective of this study was to evaluate the expression and biological role of XIST in breast cancer. The results showed that XIST was significantly down-regulated in breast cancer tissues and cell lines. Further functional analysis indicated that overexpression of XIST remarkably inhibited breast cancer cell growth, migration, and invasion. The results of luciferase reporter assays verified that miR-155 was a direct target of XIST in breast cancer. Moreover, caudal-type homeobox 1 (CDX1) was identified as a direct target of miR-155 and miR-155/CDX1 rescued the effects of XIST in breast cancer cells. Taken together, our results suggest that XIST is down-regulated in breast cancer and suppresses breast cancer cell growth, migration, and invasion via the miR-155/CDX1 axis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Loss of RapC causes defects in cytokinesis, cell migration, and multicellular development of Dictyostelium

Highlights: • We characterized the functions of RapC, an isoform of Rap1 small GTPase. • Loss of RapC causes defects in cytokinesis, cell migration, and development. • RapC plays a negative role in cell spreading and cell adhesion. • RapC is involved in tip formation from mounds during multicellular development. • This contributes to the understanding of Ras-mediated cellular processes. The small GTPase Ras proteins are involved in diverse cellular processes. We investigated the functions of RapC, one of 15 Ras subfamily GTPases in Dictyostelium. Loss of RapC resulted in a spread shape of cells; severe defects in cytokinesis leading to multinucleation; decrease of migration speed in chemoattractant-mediated cell migration, likely through increased cell adhesion; and aberrations in multicellular development producing abnormal multiple tips from one mound and multi-branched developmental structures. Defects in cells lacking RapC were rescued by expressing GFP-RapC in rapC null cells. Our results demonstrate that RapC, despite its high sequence homology with Rap1, plays a negative role in cell spreading and cell adhesion, in contrast to Rap1, which is a key regulator of cell adhesion and cytoskeleton rearrangement. In addition, RapC appears to have a unique function in multicellular development and is involved in tip formation from mounds. This study contributes to the understanding of Ras-mediated cellular processes.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MiR-30a-5p inhibits osteosarcoma cell proliferation and migration by targeting FOXD1

Highlights: • FOXD1 is overexpressed in osteosarcoma while MiR-30a-5p is lowexpressed. • MiR-30a-5p directly regulates FOXD1 by binding its 3′-UTR. • Inhibition of FOXD1 suppresses osteosarcoma cell migration and invasion. • Inhibition of FOXD1 suppresses osteosarcoma cell proliferation in vitro and in vivo. Despite a number of studies have emphasized the extensive role of microRNA (miRNA) in the development of multiple cancers, the role of miR-30a-5p in the progression of osteosarcoma (OS) and the underlying mechanism are still limited. We detected the expression level of MiR-30a-5p and forkhead box D1 (FOXD1) in Clinical OS specimens and found that miR-30a-5p was significantly decreased while FOXD1 was markedly increased. Dual luciferase assay confirmed that FOXD1 was directly regulated by miR-30a-5p. In vitro assay showed that inhibitior of FOXD1 suppressed cell proliferation, migration and invasion in MG63 and U2OS cells, while overexpression of FOXD1 promoted OS cell proliferation and migration. In vivo assay further showed the inhibition of tumor growth after knockdown of FOXD1. These results suggested that FOXD1 might play key roles in OS development and progression, and was negatively regulated by miR-30a-5p in OS.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

CCN1 accelerates re-epithelialization by promoting keratinocyte migration and proliferation during cutaneous wound healing

Highlights: • Re-epithelialization is the restoration of skin integrity following injury. • CCN family member 1 (CCN1) is upregulated in the early stages following injury. • CCN1 promotes human primary keratinocyte migration and proliferation. • Topical CCN1 application stimulates re-epithelialization in mouse burn models. • CCN1 is more potent than bFGF in initiating re-epithelialization. Re-epithelialization is an essential part of wound healing and has a prominent influence on the prognosis. CCN family member 1 (CCN1 or Cysteine-rich 61, CYR61), a matricellular protein, has a potential role in the wound healing process. However, its role in re-epithelialization remains unclear. The aim of this study was to determine the expression of CCN1 in the epidermis and its effect on keratinocytes during re-epithelialization. CCN1 expression in the wounded skin was analyzed using microarray data from GEO database and detected by immunofluorescence. The results showed upregulated CCN1 during the early stages of wound healing. Human primary keratinocytes were treated with recombinant human CCN1. The results showed that CCN1 promoted keratinocyte migration and proliferation. Moreover, a full-thickness mouse skin wound model and a superficial second-degree burn mouse model treated intracutaneously with CCN1 were used for in vivo studies. Topical treatment with CCN1 protein accelerated wound closure and re-epithelialization. Additionally, longer newly-formed epithelium tongue and elevated expression of PCNA and Ki67 were detected in the CCN1-treated group 4 days post-burn. These results indicate that CCN1 accelerates re-epithelialization by promoting keratinocyte migration and proliferation, and may serve as a novel target to promote re-epithelialization.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MYPT1 is targeted by miR-145 inhibiting viability, migration and invasion in 2D and 3D HeLa cultures

Highlights: • miR-143/145 affect viability, migration and invasion on monolayer and spheroid cultures. • miR-145 produces a stronger inhibitory effect and increases pMLC levels through MYPT1 targeting. • MYPT1 silencing by siRNAs reproduces miR-145 effects. The miR-143/145 cluster is down-regulated in cervical tumor cells suggesting a role in tumorigenesis including cytoskeleton remodeling, a key event for tumor progression. The aim of the present work was to determine the role of miR-143/145 in the modulation of the myosin regulator phospho-myosin light chain (pMLC). HeLa monolayer and tridimensional cultures were transfected with miR-143 or miR-145 mimics inhibiting cell viability, proliferation, migration and invasion, mainly through miR-145. MiR-145 transfection increased pMLC levels by targeting the MYPT1 subunit of the regulatory myosin phosphatase. MYPT1 knockdown by siRNAs reproduced miR-145 effects suggesting miR-145 as a tumor suppressor through MYPT1 targeting, leading to a subsequent increase of pMLC levels with implications for cervical cell viability, migration and invasion.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

On the moisture migration of concrete subject to high temperature with different heating rates

A better understanding of moisture migration in concrete at high temperature can play an important role to improve the fire-resistance and radiation-shielding capability of concrete structures. In this regard, within the numerical framework of Multi-physics Lattice Discrete Particle Model, the moisture clog in concrete during heating is defined as the moisture-saturated region between the so-called “water front” and “water back” (isosurfaces of saturation = 1). The moisture migration in concrete subject to slow and fast heating has been investigated by simulating experimental tests in which moisture has been monitored via different techniques, namely 3D Neutron Tomography and Ground-Penetrating Radar. An overall consistency between experimental and numerical results has been observed, indirectly proving the effectiveness of numerical modelling and experimental monitoring of moisture migration.

36 MATERIALS SCIENCE↗
DOE OSTI2025

Carboxyl-functionalized perovskite enables ALD growth of a compact and uniform ion migration barrier

Mixed-halide wide-band-gap perovskites are critical components of highly efficient tandem cells, but their operating stability is limited by halide migration. Metal oxides deposited via atomic layer deposition (ALD) have been shown to block halide migration; however, previously pursued methods result in inhomogeneous nucleation and growth. We hypothesized that functionalizing the perovskite surface with ALD-active carboxyl groups could promote nucleation and enable higher-temperature metal oxide growth. We find that 5-ammonium valeric acid iodide (5-AVAI) facilitates the formation of a compact and uniform aluminum oxide (Al 2 O 3 ) layer and allows growth at 100°C compared with the previous limit of 75°C. We demonstrate that halide migration into the C 60 electron transport layer is reduced by a factor of 10 compared with the reference case. Finally, Al 2 O 3 -capped perovskite solar cells with a band gap of 1.78 eV retain 90% of their initial power conversion efficiency after 1,000 h of continuous operation under 1-sun illumination at 55°C.

Al2O3↗
DOE OSTI2019

Approaches to multi-scale analyses of mechanically and thermally-driven migration of fluid inclusions in salt rocks

Fluid inclusions are found within mineral crystals or along grain boundaries in many sedimentary rocks, notably in evaporite formations, and can migrate along a thermal or hydro-mechanical gradient. Shale and salt rocks have been considered potential host rocks for radioactive waste disposal, due to their low permeability. Previously stagnant inclusions may become mobilised by a perturbation of the in situ state by a geotechnical installation or the emplacement of heat-generating waste. Here, the migration of fluid inclusions can thus have important impacts on the long-term performance of a geologic repository for high-level radioactive waste disposal. As a part of the international research project DECOVALEX-2019, two aspects of fluid inclusion migration in rock salt are currently investigated under different boundary conditions: a) altered hydro-mechanical conditions as a consequence of tunnel excavation or borehole drilling and b) coupled thermo-hydro-mechanical-chemical conditions during the heating period of the post-closure phase of a repository.

58 GEOSCIENCES↗
DOE OSTI2014

Zinc oxide nanoparticles induce migration and adhesion of monocytes to endothelial cells and accelerate foam cell formation

Metal oxide nanoparticles are widely used in industry, cosmetics, and biomedicine. However, the effects of exposure to these nanoparticles on the cardiovascular system remain unknown. The present study investigated the effects of nanosized TiO{sub 2} and ZnO particles on the migration and adhesion of monocytes, which are essential processes in atherosclerogenesis, using an in vitro set-up of human umbilical vein endothelial cells (HUVECs) and human monocytic leukemia cells (THP-1). We also examined the effects of exposure to nanosized metal oxide particles on macrophage cholesterol uptake and foam cell formation. The 16-hour exposure to ZnO particles increased the level of monocyte chemotactic protein-1 (MCP-1) and induced the migration of THP-1 monocyte mediated by increased MCP-1. Exposure to ZnO particles also induced adhesion of THP-1 cells to HUVECs. Moreover, exposure to ZnO particles, but not TiO{sub 2} particles, upregulated the expression of membrane scavenger receptors of modified LDL and increased cholesterol uptake in THP-1 monocytes/macrophages. In the present study, we found that exposure to ZnO particles increased macrophage cholesterol uptake, which was mediated by an upregulation of membrane scavenger receptors of modified LDL. These results suggest that nanosized ZnO particles could potentially enhance atherosclerogenesis and accelerate foam cell formation. - Highlights: • Effects of metal oxide nanoparticles on foam cell formation were investigated. • Exposure to ZnO nanoparticles induced migration and adhesion of monocytes. • Exposure to ZnO nanoparticles increased macrophage cholesterol uptake. • Expression of membrane scavenger receptors of modified LDL was also increased. • These effects were not observed after exposure to TiO{sub 2} nanoparticles.

60 APPLIED LIFE SCIENCES↗