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Effects of gold nanoparticles on vascular endothelial growth factor-A-induced melanoma cell growth and angiogenesisMatutule, Lebogang Johanna 11 1900 (has links)
Melanoma is a skin cancer that relies on angiogenesis for growth and progression. Angiogenesis is the growth of new vessels from existing vessels and follows a number of steps that include endothelial cell growth, migration and tubulogenesis. Current anti-angiogenic drugs are not effective in the treatment of melanomas due to serious side effects such as hypertension and the development of resistance. On the other hand, gold nanoparticles (AuNPs) have been reported to be biocompatible in preclinical models. Furthermore, AuNPs were shown to be cytotoxic to prostate cancer cells. In human umbilical vein endothelial cells, AuNPs inhibited the angiogenic protein, vascular endothelial growth factor-A (VEGF-A). Therefore, the study aimed to investigate the possible cytotoxic effects of AuNPs (1.2–3.2 nM) on melanoma cells and angiogenesis parameters (endothelial cell growth and migration) as well as on the levels of angiogenesis promoting proteins, VEGF-A and placental growth factor (PIGF). Melanoma (B16-F10) cells and tumour-derived endothelial (sEnd.2) cells were maintained in an incubator in a humidified atmosphere containing 5% CO2 at a temperature of 37°C. To investigate whether AuNPs were cytotoxic to melanoma cells, the effect of the particles on B16-F10 cell survival was measured using the crystal violet assay. To determine the effects of AuNPs on angiogenesis parameters, endothelial cell (EC) growth and migration were investigated using crystal violet assay and the scratch assay respectively. Also, EC morphology was studied using polarisation-optical interference contrast light microscopy. The enzyme-linked immunosorbent assay (ELISA) was used to determine the effects of AuNPs on the levels of VEGF-A and PIGF. The results showed that AuNPs decreased the viability of melanoma and endothelial cells. The scratch assay showed that more ECs migrated in cultured treated with AuNPs (P < 0.05). The concentration of VEGF-A and PIGF was reduced significantly following treatment with AuNPs, meaning that the particles exhibited anti-angiogenic properties. This outcome provides a basis for further testing of AuNPs as a potential treatment for melanoma. / Dissertation (MSc)--University of Pretoria, 2020. / National Research Foundation / Mintek / Physiology / MSc / Unrestricted
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Activation of AP-1 and SP1 Correlates With Wound Growth Factor Gene Expression in Glucan-Treated Human FibroblastsWei, Duo, Williams, David, Browder, William 28 August 2002 (has links)
Glucan is a natural product immunomodulator that has been reported to enhance early wound repair. The mechanism of glucan-stimulated wound repair was thought to be indirect via macrophage release of wound growth factors. However, recent data indicate that there are glucan-specific receptors on human fibroblasts that can modulate cellular function following interaction with the glucan ligand. In this study we examined the effect of glucan on activation of the transcription factors activator protein-1 (AP-1) and specificity protein-1 (Sp1) in normal human dermal fibroblasts. AP-1 and Sp1 are involved in the regulation of cytokine and procollagen genes. In addition, we evaluated the effect of glucan on wound growth factor and vascular endothelial growth factor (VEGF) mRNA expression in primary cultures of normal human dermal fibroblasts. Glucan (1 μg/ml) stimulated fibroblast AP-1 and Sp1 activation in a time-dependent manner, although the temporal kinetics varied between the two transcription factors. AP-1 binding activity was increased (p<0.05) at early time intervals (1, 2, 4, 8 and 12 h), while Sp1 nuclear binding activity was increased (p<0.05) at later time intervals (12, 24, 36 and 48 h). Glucan (1 μg/ml) stimulated fibroblast expression of neurotrophin 3 (NT-3), platelet derived growth factor A (PDGF-A), platelet derived growth factor B (PDGF-B), fibroblast growth factor acidic (aFGF), fibroblast growth factor basic (bFGF), transforming growth factor alpha (TGFα), transforming growth factor beta (TGFβ) and VEGF mRNA at 8 h.
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Combinational treatment approach for traumatic spinal cord injuryWalker, Melissa J. 02 March 2016 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Spinal cord injury (SCI) is devastating and debilitating, and currently no
effective treatments exist. Approximately, 12,000 new cases of SCI occur
annually in the United States alone. The central nervous system has very low
repair capability after injury, due to the toxic environment in the injured tissue.
After spinal cord trauma, ruptured blood vessels cause neighboring cells and
tissues to be deprived of oxygen and nutrients, and result in the accumulation of
carbon dioxide and waste. New blood vessels form spontaneously after SCI, but
then retract as the injured tissue forms a cavity. Thus, the newly formed
vasculature likely retracts because it lacks a structural support matrix to extend
across the lesion. Currently, in the field of spinal cord injury, combinational
treatment approaches appear to hold the greatest therapeutic potential.
Therefore, the aim of these studies was to transplant a novel, non-immunogenic,
bioengineered hydrogel, into the injured spinal cord to serve as both a structural
scaffold (for blood vessels, axons, and astrocytic processes), as well as a
functional matrix with a time-controlled release of growth factors (Vascular
endothelial growth factor, VEGF; Glial cell line-derived neurotrophic factor,
GDNF). The benefit of this hydrogel is that it remains liquid at cooler
temperatures, gels to conform to the space surrounding it at body temperature,
and was designed to have a similar tensile strength as spinal cord tissue. This is advantageous due to the non-uniformity of lesion cavities following contusive
spinal cord injury. Hydrogel alone and combinational treatment groups
significantly improved several measures of functional recovery and showed
modest histological improvements, yet did not provoke any increased sensitivity
to a thermal stimulus. Collectively, these findings suggest that with further
investigation, hydrogel along with a combination of growth factors might be a
useful therapeutic approach for repairing the injured spinal cord.
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Studies for maximizing value of antibody drugs against tumors / 抗がん治療における抗体薬の価値最大化に向けた研究Kashima(Yamashita), Yoriko 25 November 2014 (has links)
京都大学 / 0048 / 新制・論文博士 / 博士(農学) / 乙第12879号 / 論農博第2806号 / 新制||農||1028(附属図書館) / 学位論文||H26||N4878(農学部図書室) / 31597 / (主査)教授 植田 和光, 教授 植田 充美, 教授 矢﨑 一史 / 学位規則第4条第2項該当 / Doctor of Agricultural Science / Kyoto University / DFAM
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Expression of Vascular Endothelial Growth Factor in Ovarian Cancer Inhibits Tumor Immunity through the Accumulation of Myeloid-Derived Suppressor Cells / 卵巣癌における血管内皮増殖因子の発現は、骨髄由来免疫抑制性細胞の浸潤を介して腫瘍免疫を抑制しているHorikawa, Naoki 23 March 2017 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第20253号 / 医博第4212号 / 新制||医||1020(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 河本 宏, 教授 戸井 雅和, 教授 小川 誠司 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network / 乳癌においてVEGFはNRP1/ARHGAP17/Cdc42のネットワークを通じてfilopodiaの形成を促進しmigrationを誘導するKiso, Marina 26 November 2018 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第21414号 / 医博第4404号 / 京都大学大学院医学研究科医学専攻 / (主査)教授 万代 昌紀, 教授 小川 誠司, 教授 武藤 学 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Cellulose-chitosan based Scaffolds as Robust Injectable System for Bone RegenerationGaihre, Bipin 28 August 2019 (has links)
No description available.
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Inhibition of VEGF receptors induces pituitary apoplexy: an experimental study in mice / VEGF受容体の阻害は下垂体卒中を誘発する:マウスにおける実験的研究Sugita, Yoshito 23 March 2023 (has links)
京都大学 / 新制・課程博士 / 博士(医学) / 甲第24529号 / 医博第4971号 / 新制||医||1065(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 髙橋 良輔, 教授 浅野 雅秀, 教授 辻川 明孝 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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The Role of CD36 in Thrombospondin-1 Mediated Antiangiogenesis: A Study of Regulation of CD36 Ecto-phosphorylation and Mechanisms of VEGF InhibitionChu, Ling-yun 22 May 2012 (has links)
No description available.
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Study of 3'-Untranslated Region of Inducible Nitric Oxide Synthase and Identification of Other Targets of Gait PathwayVadlamani, Sirisha 02 December 2008 (has links)
No description available.
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