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High expression of the circadian gene mPer2 diminishes the radiosensitivity of NIH 3T3 cells
Chang, L.;Liu, Y.Y.;Zhu, B.;Li, Y.;Hua, H.;Wang, Y.H.;Zhang, J.;Jiang, Z.;Wang, Z.R.;
Brazilian Journal of Medical and Biological Research , 2009, DOI: 10.1590/S0100-879X2009005000022
Abstract: period2 is a core circadian gene, which not only maintains the circadian rhythm of cells but also regulates some organic functions. we investigated the effects of mperiod2 (mper2) expression on radiosensitivity in normal mouse cells exposed to 60co-γ-rays. nih 3t3 cells were treated with 12-o-tetradecanoylphorbol-13-acetate (tpa) to induce endogenous mper2 expression or transfected with pcdna3.1(+)-mper2 and irradiated with 60co-γ-rays, and then analyzed by several methods such as flow cytometry, colony formation assay, rt-pcr, and immunohistochemistry. flow cytometry and colony formation assay revealed that irradiated nih 3t3 cells expressing high levels of mper2 showed a lower death rate (tpa: 24 h 4.3% vs 12 h 6.8% and control 9.4%; transfection: pcdna3.1-mper2 3.7% vs pcdna3.1 11.3% and control 8.2%), more proliferation and clonogenic survival (tpa: 121.7 ± 6.51 vs 66.0 ± 3.51 and 67.7 ± 7.37; transfection: 121.7 ± 6.50 vs 65.3 ± 3.51 and 69.0 ± 4.58) both when treated with tpa and transfected with mper2. rt-pcr analysis showed an increased expression of bax, bcl-2, p53, c-myc, mre11, and nbs1, and an increased proportionality of bcl-2/bax in the irradiated cells at peak mper2 expression compared with cells at trough mper2 expression and control cells. however, no significant difference in rad50 expression was observed among the three groups of cells. immunohistochemistry also showed increased protein levels of p53, bax and proliferating cell nuclear antigen in irradiated cells with peak mper2 levels. thus, high expression of the circadian gene mper2 may reduce the radiosensitivity of nih 3t3 cells. for this effect, mper2 may directly or indirectly regulate the expressions of cell proliferation- and apoptosis-related genes and dna repair-related genes.
A proteomic analysis of the functional effects of fatty acids in NIH 3T3 fibroblasts
Juliana Magdalon, Elaine Hatanaka, Talita Romanatto, Hosana G Rodrigues, Wilson MT Kuwabara, Caitriona Scaife, Philip Newsholme, Rui Curi
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-218
Abstract: Found in the majority of tissues of the body, fibroblasts are responsible for the synthesis and secretion of most extracellular matrix (ECM) components, such as proteoglycans, collagens, laminin and fibronectin, which bind to proteins expressed on cell surfaces thus modulating physiologic responses. Fibroblasts can also secrete proteinases, including matrix metalloproteinases and plasminogen, hence playing an important role in ECM degradation and tissue remodeling [1-3].The dysregulation of fibroblast biology is associated with several diseases and pathological states, including deficient wound healing [4-6], pulmonary diseases [7,8], cardiovascular diseases [9,10] and cancer [11]. Therefore, the discovery of new therapies modulating fibroblast biology could be a powerful target to develop treatment against such diseases. Oleic (18:1n-9), linoleic (18:2n-6) and palmitic (16:0) acids are the most abundant fatty acids in the western diets [12]. The latter is a saturated fatty acid found in palm oil, butter, milk, cheese and meats, whereas oleic acid is a monounsaturated fatty acid found in olive oil, meat, eggs and milk and linoleic acid is a polyunsaturated fatty acid found in soybean, sunflower, safflower and corn oils. The effects of prostaglandin derived from n-3 and n-6 fatty acids on specific protein expression (e.g. COX-2 and IL-6) in NIH 3T3 fibroblasts [13] and some aspects of the impact of fatty acids on process involving fibroblast function [14-16] have been reported. However, no systematic study has assessed the pleiotropic effects of fatty acids on fibroblast protein expression. Therefore, the aim of this study was to assess the effects of oleic (OLA), linoleic (LNA) or palmitic acids (PAM) on protein expression of NIH 3T3 fibroblasts, as determined by 2D-DIGE, i.e., separation of proteins by isoelectric focusing in the first dimension followed by SDS-PAGE in the second. This approach has been successful in elucidating the actions of palmitic acid on prot
Characterization of Porcine Endogenous Retrovirus Clones from the NIH Miniature Pig BAC Library
Seong-Lan Yu,Woo-Young Jung,Kie-Chul Jung,In-Cheol Cho,Hyun-Tae Lim,Dong-Il Jin,Jun-Heon Lee
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/482568
Abstract: Pigs have been considered as donors for xenotransplantation in the replacement of human organs and tissues. However, porcine endogenous retroviruses (PERVs) might transmit new infectious disease to humans during xenotransplantation. To investigate PERV integration sites, 45 PERV-positive BAC clones, including 12 PERV-A, 16 PERV-B, and 17 PERV-C clones, were identified from the NIH miniature pig BAC library. The analysis of 12 selected full-length sequences of PERVs, including the long terminal repeat (LTR) region, identified the expected of open reading frame length, an indicative of active PERV, in all five PERV-C clones and one of the four PERV-B clones. Premature stop codons were observed in only three PERV-A clones. Also, eleven PERV integration sites were mapped using a 5000-rad IMpRH panel. The map locations of PERV-C clones have not been reported before, thus they are novel PERV clones identified in this study. The results could provide basic information for the elimination of site-specific PERVs in selection of pigs for xenotransplantation.
海参肽的分离纯化及其对NIH/3T3细胞胶原蛋白分泌的影响  [PDF]
- , 2017, DOI: 10.13982/j.mfst.1673-9078.2017.3.004
Abstract: 本论文从刺参中分离纯化得到一种海参肽,并研究其对NIH/3T3细胞增殖和胶原蛋白分泌的影响。采用活性追踪的方法从新鲜刺参中通过离子交换层析、凝胶层析分离纯化得到海参肽SP12,采用MTT法检测SP12对NIH/3T3细胞的增殖作用;采用流式细胞术检测SP12对NIH/3T3细胞细胞周期的影响;采用羟脯氨酸测定试剂盒的方法检测SP12对NIH/3T3细胞胶原蛋白分泌的影响;采用Western Blot及RT-PCR的方法,在蛋白水平及基因水平上检测SP12对NIH/3T3细胞I型胶原蛋白、MMP-1及TIMP-1表达的影响。结果表明SP12能显著提高NIH/3T3细胞的增殖率,能促进NIH/3T3细胞由G1期向S期转变,增加其胶原蛋白的分泌量,且在0~20 μg/mL范围内均呈剂量依赖性。在蛋白水平和基因水平,SP12均能显著促进I型胶原蛋白及TIMP-1的表达,抑制MMP-1的表达,这可能是SP12促进NIH/3T3细胞胶原蛋白分泌的作用机制。
A sea cucumber peptide, SP12, was isolated and purified from Stichopus japonicus, and its impact on NIH/3T3 cell proliferation and secretion of type I collagen was studied. SP12 was purified by ion exchange chromatography and gel filtration chromatography from fresh Stichopus japonicus using a cell activity tracking method. The effect of SP12 on NIH/3T3 cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and its impact on cell cycle progression was determined by flow cytometry. The effect of SP12 on collagen secretion by NIH/3T3 cells was measured by hydroxyproline kit, and its impact on the expression of type I collagen, matrix metalloproteinase-1 (MMP-1), and tissue inhibitor of metalloproteinases-1 (TIMP-1) in NIH/3T3 cells was measured at the protein and gene levels by western blot and reverse-transcription polymerase chain reaction (RT-PCR). The results clearly demonstrate that SP12 can considerably enhance the proliferation rate of NIH/3T3 cells and promote progression from G1 phase to S phase. In a range of 0~20 μg/mL, SP12 enhanced collagen secretion by NIH/3T3 cells in a dose-dependent manner. At the protein and genetic levels, SP12 considerably promoted the expression of type I collagen and TIMP-1, and inhibited the expression of MMP-1; this might be the mechanism underlying SP12 promotion of collagen secretion by NIH/3T3 cells.
染料木黄酮对NIH/3T3细胞体外短期转化实验的影响  [PDF]
中国公共卫生 , 2002, DOI: 10.11847/zgggws2002-18-011-26
Abstract: ?目的通过观察染料木黄酮对NIH/3T3细胞体外恶性转化的影响,研究染料木黄酮在癌症起始阶段的预防作用.方法体外短期转化实验.结果染料木黄酮在对细胞无明显毒性的浓度下,对MNNG所诱发NIH/3T3细胞恶性转化有明显的抑制作用,其最低抑制浓度为37μmol/L.结论染料木黄酮可能是化学致癌过程的抑制剂.
Weaving Frames  [PDF]
Travis Bemrose,Peter G. Casazza,Karlheinz Gr?chenig,Mark C. Lammers,Richard G. Lynch
Mathematics , 2015,
Abstract: We study an intriguing question in frame theory we call "Weaving Frames" that is partially motivated by preprocessing of Gabor frames. Two frames $\{\varphi_i\}_{i\in I}$ and $\{\psi_i \}_{i\in I}$ for a Hilbert space ${\mathbb H}$ are woven if there are constants $0
Ultraviolet C Irradiation Induces Different Expression of Cyclooxygenase 2 in NIH 3T3 Cells and A431 Cells: The Roles of COX-2 Are Different in Various Cell Lines  [PDF]
Ming-Hong Tai,Chien-Hui Weng,Dir-Pu Mon,Chun-Yi Hu,Ming-Hsiu Wu
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms13044351
Abstract: Ultraviolet C (UVC) is a DNA damage inducer, and 20 J/m 2 of UVC irradiation caused cell growth inhibition and induced cell death after exposure for 24–36 h. The growth of NIH 3T3 cells was significantly suppressed at 24 h after UVC irradiation whereas the proliferation of A431 cells was inhibited until 36 h after UVC irradiation. UVC irradiation increased COX-2 expression and such up-regulation reached a maximum during 3–6 h in NIH 3T3 cells. In contrast, UVC-induced COX-2 reached a maximum after 24–36 h in A431 cells. Measuring prostaglandin E2 (PGE2) level showed a biphasic profile that PGE2 release was rapidly elevated in 1–12 h after UVC irradiation and increased again at 24 h in both cell lines. Treatment with the selective COX-2 inhibitor, SC-791, during maximum expression of COX-2 induction, attenuated the UVC induced-growth inhibition in NIH 3T3 cells. In contrast, SC-791 treatment after UVC irradiation enhanced death of A431 cells. These data showed that the patterns of UVC-induced PGE2 secretion from NIH 3T3 cells and A431 cells were similar despite the differential profile in UVC-induced COX-2 up-regulation. Besides, COX-2 might play different roles in cellular response to UVC irradiation in various cell lines.
Weaving Lao Silk Into Indigo Nights
Melody Kemp
Asia-Pacific Journal : Japan Focus , 2010,
Abstract: The air turned chilly as the sun sighed into the nearby hills. It picked up the smells of dust mixed with metallic and dung flavours. Miss Phaeng watched, holding her breath as the last sliver of red fell out of sight. Casting a quick mantra to the spirits of nature, she swallowed a glass of lao lao to start the evening.Leaning mindfully over her loom, Miss Phaeng raked her nails across the piano strings of silk warp, plucking each to test its tension. A black sheet of pin-straight hair fell over her face, hiding the claret birthmark shaped just like a spider, that crept over her right cheek, one leg disappearing into the fine hairs of her temple.The coarse ivory silk recently spooled from the cocoons gathered in her garden pushed back against her hand.She felt the fizz of anticipation low in her belly as she gathered all the many shuttles holding the weft silk and dumped them into an old blackened basket. Inhaling its heady stink of ash, grass and smoke, she placed the basket next to where she would sit.Melody Kemp offers a close look at the Lao silk industry.
Romidepsin inhibits Ras-dependent growth transformation of NIH 3T3 fibroblasts and RIE-1 epithelial cells independently of Ras signaling inhibition
Ariella B Hanker, Kevin D Healy, Jean Nichols, Channing J Der
Journal of Molecular Signaling , 2009, DOI: 10.1186/1750-2187-4-5
Abstract: To rigorously assess romidepsin as an antagonist of Ras, we utilized two well-characterized cell models for Ras transformation. We found that romidepsin blocked the anchorage-dependent and -independent growth of NIH 3T3 fibroblasts and RIE-1 epithelial cells transformed by all three Ras isoforms. However, romidepsin treatment also blocked growth transformation caused by other oncoproteins (B-Raf and ErbB2/Neu), suggesting that romidepsin is not selective for Ras. We also observed striking differences in romidepsin-mediated growth inhibition between transformed NIH 3T3 fibroblasts compared to RIE-1 epithelial cells, suggesting that the mechanism by which romidepsin blocks transformation is dependent on cellular context. Finally, we found that romidepsin did not inhibit Ras activation of the ERK and AKT effector pathways in NIH 3T3 and RIE-1 cells, suggesting that romidepsin does not directly antagonize Ras.Taken together, our results suggest that romidepsin is not selective for Ras-transformed cells and that the anti-tumor activity of romidepsin is not due to direct inhibition of Ras function.Romidepsin (also called FK228, depsipeptide) is a bicyclic depsipeptide that was isolated from Chromobacterium violaceum and potently inhibits tumor growth [1,2]. The histone deacetylase (HDAC) family of enzymes was identified as the biologic target of romidepsin [3]. Romidepsin is a potent inhibitor of class I HDACs and, to a lesser extent, inhibits class II HDACs [4]. HDACs are involved in chromatin remodeling and transcriptional silencing, including the epigenetic silencing of several tumor suppressors [5]. Altered HDAC activity has been found in several cancers [5,6] and HDAC inhibitors have been shown to reverse cancer-associated epigenetic changes and cause growth arrest, differentiation, and apoptosis in cancer cell lines [6]. Therefore, romidepsin and other HDAC inhibitors have emerged as promising therapeutics for the treatment of cancer [4,6-8]. Presently, romidepsin a
Phenotypic and Genotypic Characteristics of Novel Mouse Cell Line (NIH/3T3)-Adapted Human Enterovirus 71 Strains (EV71:TLLm and EV71:TLLmv)  [PDF]
Carla Bianca Luena Victorio, Yishi Xu, Qimei Ng, Vincent T. K. Chow, Kaw Bing Chua
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092719
Abstract: Since its identification in 1969, Enterovirus 71 (EV71) has been causing periodic outbreaks of infection in children worldwide and most prominently in the Asia-Pacific Region. Understanding the pathogenesis of Enterovirus 71 (EV71) is hampered by the virus’s inability to infect small animals and replicate in their derived in vitro cultured cells. This manuscript describes the phenotypic and genotypic characteristics of two selected EV71 strains (EV71:TLLm and EV71:TLLmv), which have been adapted to replicate in mouse-derived NIH/3T3 cells, in contrast to the original parental virus which is only able to replicate in primate cell lines. The EV71:TLLm strain exhibited productive infection in all primate and rodent cell lines tested, while EV71:TLLmv exhibited greater preference for mouse cell lines. EV71:TLLmv displayed higher degree of adaptation and temperature adaptability in NIH/3T3 cells than in Vero cells, suggesting much higher fitness in NIH/3T3 cells. In comparison with the parental EV71:BS strain, the adapted strains accumulated multiple adaptive mutations in the genome resulting in amino acid substitutions, most notably in the capsid-encoding region (P1) and viral RNA-dependent RNA polymerase (3D). Two mutations, E167D and L169F, were mapped to the VP1 canyon that binds the SCARB2 receptor on host cells. Another two mutations, S135T and K140I, were located in the VP2 neutralization epitope spanning amino acids 136–150. This is the first report of human EV71 with the ability to productively infect rodent cell lines in vitro.
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