The effect of pH on cell viability, cell migration, cell proliferation, wound closure, and wound reepithelialization: In vitro and in vivo study

2017 ◽  
Vol 25 (2) ◽  
pp. 260-269 ◽  
Author(s):  
Carla R. Kruse ◽  
Mansher Singh ◽  
Stefan Targosinski ◽  
Indranil Sinha ◽  
Jens A. Sørensen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Viability ◽  
Wound Closure ◽  
In Vivo Study ◽  
Effect Of Ph

scholarly journals Resveratrol Enhances Inhibition Effects of Cisplatin on Cell Migration and Invasion and Tumor Growth in Breast Cancer MDA-MB-231 Cell Models In Vivo and In Vitro

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2204
Author(s):  
Meng-Die Yang ◽  
Yang Sun ◽  
Wen-Jun Zhou ◽  
Xiao-Zheng Xie ◽  
Qian-Mei Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Cell Viability ◽  
Synergistic Effects ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tgf Β1

Triple-negative breast cancer (TNBC) is a refractory type of breast cancer that does not yet have clinically effective drugs. The aim of this study is to investigate the synergistic effects and mechanisms of resveratrol combined with cisplatin on human breast cancer MDA-MB-231 (MDA231) cell viability, migration, and invasion in vivo and in vitro. In vitro, MTS assays showed that resveratrol combined with cisplatin inhibits cell viability as a concentration-dependent manner, and produced synergistic effects (CI < 1). Transwell assay showed that the combined treatment inhibits TGF-β1-induced cell migration and invasion. Immunofluorescence assays confirmed that resveratrol upregulated E-cadherin expression and downregulated vimentin expression. Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-β1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. In vivo, resveratrol enhanced tumor growth inhibition and reduced body weight loss and kidney function impairment by cisplatin in MDA231 xenografts, and significantly reduced the expressions of P-AKT, P-PI3K, Smad2, Smad3, P-JNK, P-ERK, and NF-κB in tumor tissues (p < 0.05). These results indicated that resveratrol combined with cisplatin inhibits the viability of breast cancer MDA231 cells synergistically, and inhibits MDA231 cells invasion and migration through Epithelial-mesenchymal transition (EMT) approach, and resveratrol enhanced anti-tumor effect and reduced side of cisplatin in MDA231 xenografts. The mechanism may be involved in the regulations of PI3K/AKT, JNK, ERK and NF-κB expressions.

scholarly journals DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Yixin Tong ◽  
Yuan Huang ◽  
Yuchao Zhang ◽  
Xiangtai Zeng ◽  
Mei Yan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Downstream Target ◽  
Normal Tissues ◽  
Physiological Processes ◽  
Mutual Regulation

AbstractAt present, colorectal cancer (CRC) has become a serious threat to human health in the world. Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent hydrolase that may be involved in several physiological processes. However, whether DPP3 affects the development and progression of CRC remains a mystery. This study is the first to demonstrate the role of DPP3 in CRC. Firstly, the results of immunohistochemistry analysis showed the upregulation of DPP3 in CRC tissues compared with normal tissues, which is statistically analyzed to be positively correlated with lymphatic metastasis, pathological stage, positive number of lymph nodes. Moreover, the high expression of DPP3 predicts poor prognosis in CRC patients. In addition, the results of cell dysfunction experiments clarified that the downregulation of DPP3 significantly inhibited cell proliferation, colony formation, cell migration, and promoted apoptosis in vitro. DPP3 depletion could induce cell apoptosis by upregulating the expression of BID, BIM, Caspase3, Caspase8, HSP60, p21, p27, p53, and SMAC. In addition, downregulation of DPP3 can reduce tumorigenicity of CRC cells in vivo. Furthermore, CDK1 is determined to be a downstream target of DPP3-mediated regulation of CRC by RNA-seq, qPCR, and WB. The interaction between DPP3 and CDK1 shows mutual regulation. Specifically, downregulation of DPP3 can accentuate the effects of CDK1 knockdown on the function of CRC cells. Overexpression of CDK1 alleviates the inhibitory effects of DPP3 knockdown in CRC cells. In summary, DPP3 has oncogene-like functions in the development and progression of CRC by targeting CDK1, which may be an effective molecular target for the prognosis and treatment of CRC.

Cell migration, viability and tissue reaction of calcium hypochlorite based-solutions irrigants: An in vitro and in vivo study

2017 ◽  
Vol 73 ◽  
pp. 34-39 ◽  
Author(s):  
Gabriela Bess Ferraz Blattes ◽  
Leticia Boldrin Mestieri ◽  
Daiana Elisabeth Böttcher ◽  
Anna Cristina Medeiros Fossati ◽  
Francisco Montagner ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tissue Reaction ◽  
In Vivo Study ◽  
Calcium Hypochlorite

scholarly journals Apigenin Protects the Brain against Ischemia/Reperfusion Injury via Caveolin-1/VEGF In Vitro and In Vivo

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Qiongyi Pang ◽  
Yun Zhao ◽  
Xiang Chen ◽  
Kaiyi Zhao ◽  
Qiongxiang Zhai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tube Formation ◽  
Caveolin 1 ◽  
The Brain

Apigenin is a natural flavonoid found in several dietary plant foods as vegetables and fruits. To investigate potential anti-ischemia/reperfusion injury properties of apigenin in vitro, cell proliferation assay, tube formation, cell migration, apoptosis, and autophagy were performed in human brain microvascular endothelial cells (HBMVECs) after oxygen-glucose deprivation/reoxygenation (OGD/R). The effect of apigenin was also explored in rats after middle cerebral artery occlusion/reperfusion (MCAO/R) via neurobehavioral scores, pathological examination, and measurement of markers involved in ischemia/reperfusion injury. Data in vitro indicated that apigenin could prompt cell proliferation, tube formation, and cell migration while inhibiting apoptosis and autophagy by affecting Caveolin-1/VEGF, Bcl-2, Caspase-3, Beclin-1, and mTOR expression. Results in vivo showed that apigenin significantly reduced neurobehavioral scores and volume of cerebral infarction while prompting vascular endothelial cell proliferation by upregulating VEGFR2/CD34 double-labeling endothelial progenitor cell (EPC) number and affecting Caveolin-1, VEGF, and eNOS expression in brain tissue of MCAO/R rats. All the data suggested that apigenin may be protective for the brain against ischemia/reperfusion injury by alleviating apoptosis and autophagy, promoting cell proliferation in HBMVECs of OGD/R, and attenuating brain damage and improved neurological function in rats of MCAO/R through the Caveolin-1/VEGF pathway.

scholarly journals Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Yongshun Li ◽  
Changrong Huang ◽  
Qizhou Bai ◽  
Jun Yu
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Tissues ◽  
Esophageal Cancer Cells ◽  
E Cadherin

AbstractEsophageal cancer is a common digestive tract cancer, which is a serious threat to human health. Ribophorin II (RPN2) is a part of an N-oligosaccharyltransferase complex, which is excessively expressed in many kinds of cancers. In the present study, we explore the biological role of RNP2 in esophageal cancer. First, we found that the expression of RPN2 was higher in esophageal cancer tissues than in adjacent non-tumor tissues, and negatively correlated with E-cadherin expression. RPN2 expression levels in esophageal cancer tissues were positively associated with differentiation and tumor node metastasis (TNM) stage. Furthermore, the expression of RPN2 was increased significantly in esophageal cancer cell lines compared with normal cells. The effect of RPN2 down-regulation on cell proliferation, cell migration, and cell invasion was examined by cell counting kit-8 (CCK8), wound healing assay, and Transwell assay, respectively. Silencing RPN2 effectively inhibited cell proliferation of esophageal cancer cells in vitro and in vivo. Cell migration and invasion were also weakened dramatically by siRPN2 treatment of esophageal cancer cells. In addition, protein expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP-2), and E-cadherin in esophageal cancer cells was determined by Western blot analysis. PCNA, MMP-2, E-cadherin, Snail and phosphorylation-Smad2/3 expression was also regulated notably by siRPN2 treatment. These findings indicate that RPN2 exhibits oncogenetic capabilities in esophageal cancer, which could provide novel insights into esophageal cancer prevention and treatment.

scholarly journals In Vitro and In Vivo Study of Titanium Grade IV and Titanium Grade V Implants with Different Surface Treatments

Metals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 449 ◽  
Author(s):  
Rosa-Maria Diaz-Sanchez ◽  
Alvaro de-Paz-Carrion ◽  
Maria-Angeles Serrera-Figallo ◽  
Daniel Torres-Lagares ◽  
Angel Barranco ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Histological Study ◽  
Surface Treatments ◽  
In Vivo Study ◽  
Positive Trend ◽  
Similar Response ◽  
Micro Ct ◽  
Titanium Grade

The aim of our study is to evaluate different implant surface treatments using TiIV and TiV in in vitro and in vivo studies. An in vitro study was established comprising four study groups with treated and untreated TiIV titanium discs (TiIVT and TiIVNT) and treated and untreated TiV titanium discs (TiVT and TiVNT). The surface treatment consisted in a grit blasting treatment with alumina and double acid passivation to modify surface roughness. The surface chemical composition and the surface microstructure of the samples were analyzed. The titanium discs were subjected to cell cultures to determine cell adhesion and proliferation of osteoblasts on them. The in vivo study was carried out on the tibia of three New Zealand rabbits in which 18 implants divided into three experimental groups were placed (TiIVT, TiIVNT, and TiVT). Micro-computed tomography (micro-CT) was performed to determine bone density around the implants. The results showed that cell culture had minor adhesion and cell proliferation in TiIVT and TiVT within the first 6 and 24 h. However, no differences were found after 48 h. No statistically significant differences were found in the in vivo micro-CT and histological study; however, there was a positive trend in bone formation in the groups with a treated surface. Conclusions: All groups showed a similar response to in vitro cell proliferation cultures after 48 h. No statistically significant differences were found in the in vivo micro-CT and histological study.

scholarly journals Neuropeptide Substance P Enhances Skin Wound Healing In Vitro and In Vivo under Hypoxia

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 222
Author(s):  
Suneel Kumar ◽  
Yuying Tan ◽  
Francois Berthiaume
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Substance P ◽  
Wound Closure ◽  
Skin Wound ◽  
Skin Wound Healing ◽  
Male And Female ◽  
Low Serum

Pressure ulcers (PUs) or sores are a secondary complication of diabetic neuropathy and traumatic spinal cord injury (SCI). PUs tend to occur in soft tissues located around bony prominences and may heal slowly or not at all. A common mechanism underlying impaired healing of PUs may be dysfunction of the local neurovascular system including deficiency of essential neuropeptides, such as substance P (SP). Previous studies indicate that disturbance in cutaneous sensory innervation leads to a defect in all stages of wound healing, as is the case after SCI. It is hypothesized that nerve fibers enhance wound healing by promoting initial inflammation via the releasing of neuropeptides such as SP. Therefore, we investigated whether exogenous SP improves skin wound healing using in vitro and in vivo models. For in vitro studies, the effects of SP on keratinocyte proliferation and wound closure after a scratch injury were studied under normoxia (pO2 ~21%) or hypoxia (pO2 ~1%) and in presence of normal serum (10% v/v) or low serum (1% v/v) concentrations. Hypoxia and low serum both significantly slowed cell proliferation and wound closure. Under combined low serum and hypoxia, used to mimic the nutrient- and oxygen-poor environment of chronic wounds, SP (10−7 M) significantly enhanced cell proliferation and wound closure rate. For in vivo studies, two full-thickness excisional wounds were created with a 5 mm biopsy punch on the dorsum on either side of the midline of 15-week-old C57BL/6J male and female mice. Immediately, wounds were treated topically with one dose of 0.5 μg SP or PBS vehicle. The data suggest a beneficial role in wound closure and reepithelization, and thus enhanced wound healing, in male and female mice. Taken together, exogenously applied neuropeptide SP enhanced wound healing via cell proliferation and migration in vitro and in vivo. Thus, exogenous SP may be a useful strategy to explore further for treating PUs in SCI and diabetic patients.

scholarly journals Dark Sweet Cherry (Prunus avium) Anthocyanins Inhibited the Growth and Biomarkers for Breast Cancer Growth and Invasion in Highly Metastatic 4T1 Tumor Cells

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 279-279
Author(s):  
Ana Carolina Silveira Rabelo ◽  
Shirley Arbizu ◽  
Maria Angelica Miglino ◽  
Susanne Talcott ◽  
Giuliana Noratto
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cell Viability ◽  
Prunus Avium ◽  
Epithelial Mesenchymal Transition ◽  
Dose Range ◽  
Mesenchymal Transition ◽  
4T1 Cells

Abstract Objectives To investigate the mechanisms underlying the breast cancer anti-invasive activity of DSC phenolics enriched in anthocyanins (ACN) in vitro and their potential in vivo. Methods 4T1 cells were treated with ACN extracted from DSC concentrate juice (FruitSmart, Grandview, WA) within dose range 20–80 µg cyanidin 3-glucoside equivalent (C3G)/mL to assess reactive oxygen species (ROS) levels using carboxy-H2DFFDA probe and cell viability using the resazurin kit (Sigma-Aldrich, St Louis, MO). Protein and mRNA expression were investigated using standard procedures and cell migration by wound healing assay. The pilot in vivo study was performed with 4T1 cells orthotopically injected into mammary fat pads of BALB/c mice (Envigo, Houston, TX, USA) (n = 4). After tumor growth, animals were gavaged with ACN (150 mg C3G/kg body weight/day, n = 2) or saline solution (control, n = 2) for one week followed by euthanasia and collection of tumors, lungs, and liver tissues for analyses. Results ACN induced ROS production (up to 5.13-fold of control) and inhibited cell viability by 50% (IC50) at 58.6 µg C3G/mL. The ACN (IC50 dose) treatment downregulated phospho-ERK1/2 and upregulated phospho-p38 proteins, linked to cell growth inhibition and caspase-dependent apoptosis mediated by the increase in cleaved/total caspase-3 protein ratio (∼3-fold of control) and suppression of total PARP (∼0.4-fold of control). ACN also suppressed the Akt/mTOR/CREB pathway that promotes proliferation and invasion. 4T1 cell migration was inhibited by 22%, consistent with the phospho-Src downregulation (down to ∼ 0.25-fold of control), that regulate epithelial-mesenchymal transition. Phospho-ERK1/2 and phospho-CREB were downregulated in mice tumors. This was accompanied by the downregulation of Cenpf mRNA in liver and lungs, which correlates with poor prognosis and metastasis, thus supporting the in vitro findings. Conclusions ACN provides a dietary alternative to fight human breast cancer invasion by incorporating DSC into the diet. More studies are guarantee to help improve the quality of life of breast cancer patients. Funding Sources This work was supported by the Northwest Cherry Growers. The authors thank the support of Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Brazil for providing Ana Carolina Silveira Rabelo the scholarship.

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