Free Shipping on orders over 50$

British Pound Sterling - GBP Euro - EUR US Dollar - USD (EUR)

Welcom to Gentaur Biotech Products!

MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS

Be the first to review this product

Availability: In stock

€80.93
OR

Quick Overview

[#ABS10508] MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS

Details

ABS10508 | MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS, 25 µg
More informations about MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS in Antibody-antibodies.com

Product Tags

Use spaces to separate tags. Use single quotes (') for phrases.

(1) 6-Hydroxydopamine induces secretion of PARK7/DJ-1 via autophagy-based unconventional secretory pathway.[TOP]

Pubmed ID :30112966
Publication Date : //
PARK7/DJ-1 is a Parkinson disease- and cancer-associated protein that functions as a multifunctional protein involved in gene transcription regulation and anti-oxidative defense. Although PARK7 lacks the secretory signal sequence, it is secreted and plays important physiological and pathophysiological roles. Whereas secretory proteins that lack the endoplasmic reticulum-targeting signal sequence are secreted from cells by way of what is called the unconventional secretion mechanism, the specific processes responsible for causing PARK7 to be secreted across the plasma membrane have remained unclear. In the present study, we found that PARK7 secretion was increased by treatment with 6-OHDA via the unconventional secretory pathway in human neuroblastoma SH-SY5Y cells and MEF cells. We also found that 6-OHDA-induced PARK7 secretion was suppressed in Atg5-, Atg9-, or Atg16l1-deficient MEF cells or ATG16L1 knockdown SH-SY5Y cells, indicating that the autophagy-based unconventional secretory pathway is involved in PARK7 secretion. We moreover observed that 6-OHDA-derived electrophilic quinone induced oxidative stress as indicated by a decrease in glutathione levels, and that this was suppressed by pretreatment with antioxidant NAC. We further found that NAC treatment suppressed autophagy and PARK7 secretion. We also observed that 6-OHDA-induced autophagy was associated with activation of AMPK and ULK1 via a pathway which was independent of MTOR. Collectively these results suggest that electrophilic 6-OHDA quinone enhances oxidative stress, and that this is followed by AMPK-ULK1 pathway activation and induction of secretory autophagy to produce unconventional secretion of PARK7.

Authors : Urano Yasuomi, Mori Chinatsu, Fuji Ayano, Konno Keito, Yamamoto Takayuki, Yashirogi Shohei, Ando Mayu, Saito Yoshiro, Noguchi Noriko,



(2) Antidepressive and anxiolytic effects of ostruthin, a TREK-1 channel activator.[TOP]

Pubmed ID :30110354
Publication Date : //
We screened a library of botanical compounds purified from plants of Vietnam for modulators of the activity of a two-pore domain K+ channel, TREK-1, and we identified a hydroxycoumarin-related compound, ostruthin, as an activator of this channel. Ostruthin increased whole-cell TREK-1 channel currents in 293T cells at a low concentration (EC50 = 5.3 μM), and also activity of the TREK-2 channel (EC50 = 3.7 mM). In contrast, ostruthin inhibited other K+ channels, e.g. human ether-à-go-go-related gene (HERG1), inward-rectifier (Kir2.1), voltage-gated (Kv1.4), and two-pore domain (TASK-1) at higher concentrations, without affecting voltage-gated potassium channel (KCNQ1 and 3). We tested the effect of this compound on mouse anxiety- and depression-like behaviors and found anxiolytic activity in the open-field, elevated plus maze, and light/dark box tests. Of note, ostruthin also showed antidepressive effects in the forced swim and tail suspension tests, although previous studies reported that inhibition of TREK-1 channels resulted in an antidepressive effect. The anxiolytic and antidepressive effect was diminished by co-administration of a TREK-1 blocker, amlodipine, indicating the involvement of TREK-1 channels. Administration of ostruthin suppressed the stress-induced increase in anti-c-Fos immunoreactivity in the lateral septum, without affecting immunoreactivity in other mood disorder-related nuclei, e.g. the amygdala, paraventricular nuclei, and dorsal raphe nucleus. Ostruthin may exert its anxiolytic and antidepressive effects through a different mechanism from current drugs.

Authors : Joseph Ancy, Thuy Tran Thi Thu, Thanh Le Tat, Okada Masayoshi,



(3) An injectable and physical levan-based hydrogel as a dermal filler for soft tissue augmentation.[TOP]

Pubmed ID :30109875
Publication Date : //
The use of injectable materials as a biofiller for soft tissue augmentation has been increasing worldwide. Levan is a biocompatible and inexpensive polysaccharide with great potential in biomaterial applications, but it has not been extensively studied. In this study, we evaluated the potential of levan as a new material for dermal fillers and prepared an injectable and physical levan-based hydrogel by combining levan with Pluronic and carboxymethyl cellulose (CMC). A sol state was prepared by mixing the polymers in a specific ratio at 4 °C for 2 days and the hydrogel was formed by increasing the temperature to 37 °C. The elastic modulus of the levan hydrogel was higher than that of a hyaluronic acid (HA)-based hydrogel. The SEM images of the levan hydrogel showed an interconnected porous structure, similar to the HA hydrogel. Levan showed non-cytotoxicity, enhanced cell proliferation, and higher amount of collagen synthesis in human dermal fibroblast cells compared to HA. The injected levan hydrogel was biocompatible and stable over 2 weeks in vivo, longer than the Pluronic F127 hydrogel or HA hydrogel. Also, the levan hydrogel showed a higher amount of collagen production than the HA hydrogel in vivo. More importantly, the levan hydrogel showed enhanced anti-wrinkle efficacy compared to the HA hydrogel in a wrinkle model mouse. Thus, the levan hydrogel with injectability, biocompatibility, and an anti-wrinkle effect has high potential as an alternative to existing commercial dermal fillers.

Authors : Choi Won Il, Hwang Youngmin, Sahu Abhishek, Min Kiyoon, Sung Daekyung, Tae Giyoong, Chang Jeong Ho,



(4) Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis.[TOP]

Pubmed ID :30109812
Publication Date : //
The p53 protein is a key tumor suppressor in mammals. In response to various forms of genotoxic stress p53 stimulates expression of genes whose products induce cell cycle arrest and/or apoptosis. An E3-ubiquitin ligase, Mdm2 (mouse-double-minute 2) and its human ortholog Hdm2, physically interact with the amino-terminus of p53 to mediate its ubiquitin-mediated degradation via the proteasome. Thus, pharmacological inhibition of the p53-Mdm2 interaction leads to overall stabilization of p53 and stimulation of its anti-tumorigenic activity. In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (ISMBDs) that stabilize p53 on the protein level. The likely mechanism behind their positive effect on p53 is mediated via the competitive interaction with Mdm2. Importantly, unlike Nutlin, these compounds selectively promoted p53-mediated cell death. These novel pharmacological activators of p53 can serve as valuable molecular tools for probing p53-positive tumors and set up the stage for development of new anti-cancer drugs.

Authors : Fedorova Olga, Daks Alexandra, Petrova Varvara, Petukhov Alexey, Lezina Larissa, Shuvalov Oleg, Davidovich Pavel, Kriger Darya, Lomert Ekaterina, Tentler Dmitry, Kartsev Victor, Uyanik Burhan, Tribulovich Vyacheslav, Demidov Oleg, Melino Gerry, Barlev Nickolai A,



(5) Apatinib targets both tumor and endothelial cells in hepatocellular carcinoma.[TOP]

Pubmed ID :30109780
Publication Date : //
Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed malignancies worldwide with poor prognosis and tends to be hypervascular. Aberrant expression of the vascular endothelial growth factor 2 (VEGFR-2) has been implicated in the progression of HCC and represents a valid target for anticancer therapy. Apatinib, a small molecule inhibitor of VEGFR-2 tyrosine kinase, shows strong antitumor activity in various tumors. This study is designed to evaluate the activity of apatinib on both human umbilical vein vascular endothelial cells (HUVECs) and HCC cell lines (in vitro and in vivo), and also to investigate the characteristics and possible mechanisms underlying these effects by molecular biology methods. Following the results in our study, apatinib inhibited phosphorylation of VEGFR-2 in HUVECs and blocked in vitro endothelial cell migration and tube formation. Concentration-dependent antiproliferative effects of apatinib were also observed in all 6 HCC cell lines including SK-Hep-1, HepG2, Hep3B, Huh-7, PLC/PRF/5, SMMC-7721. Moreover, response to apatinib of HCC cell lines was significantly correlated with VEGFR-2 expression level. Additionally, apatinib significantly inhibit VEGF-triggered VEGFR-2 phosphorylation and activation of downstream signaling molecules such as Akt and ERK1/2 in HCCs. Apatinib can also induce a cell cycle arrest at G2/M phase and promote HCC apoptosis tested in vitro. In vivo data showed that apatinib can effectively inhibit tumor growth, decreased angiogenesis, as well as induced HCC apoptosis (in some tumors), and thus prolonged animal survival in a mouse xenograft model of human HCC. Our findings suggested that apatinib is a highly potent, oral active anti-angiogenic, and anti-HCC agent. The results from current study provide a clear biological rationale to evaluate apatinib as a new agent in HCC in clinical setting, especially for the VEGFR-2 overexpression ones.

Authors : Yang Chaoxu, Qin Shukui,



(6) Effects on tumor growth and immunosuppression of a modified Tα1 peptide along with its circular dichroism spectroscopy data.[TOP]

Pubmed ID :30109250
Publication Date : //
The data presented in this article are related to the research article entitled "Immunomodulatory and Enhanced Antitumor Activity of a Modified Thymosin α1 in Melanoma and Lung Cancer" (Wang et al., 2018). Tα1 has been evaluated as effective in cancer treatment. In order to make it capable to target tumor, a peptide iRGD was introduced to Tα1. The anti-tumor activity was accessed by constructing in vivo melanoma and human non-small-cell lung cancer models treated with Tα1-iRGD to measure the tumor volume over time and tumor weight at the last day. The concentration of IFN-γ and IL-2 in C57BL/6 mice peripheral blood was determined by ELISA. And the immunomodulatory ability of Tα1-iRGD was evaluated in vivo by thymus index and spleen index. Those functions this paper was aimed at may have relationship with its secondary structure, so the circular dichroism spectra of Tα1, iRGD and Tα1-iRGD was performed.

Authors : Wang Fanwen, Li Bin, Fu Pengcheng, Li Qingqing, Zheng Heng, Lao Xingzhen,



(7) Garlic-derived compound -allylmercaptocysteine inhibits hepatocarcinogenesis through targeting LRP6/Wnt pathway.[TOP]

Pubmed ID :30109182
Publication Date : //
Whether and how garlic-derived -allylmercaptocysteine (SAMC) inhibits hepatocellular carcinoma (HCC) is largely unknown. In the current study, the role of low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) in HCC progression and the anti-HCC mechanism of SAMC was examined in clinical sample, cell model and xenograft/orthotopic mouse models. We demonstrated that SAMC inhibited cell proliferation and tumorigenesis, while induced apoptosis of human HCC cells without influencing normal hepatocytes. SAMC directly interacted with Wnt-pathway co-receptor LRP6 on the cell membrane. LRP6 was frequently over-expressed in the tumor tissue of human HCC patients (66.7% of 48 patients) and its over-expression only correlated with the over-expression of -catenin, but not with age, gender, tumor size, stage and metastasis. Deficiency or over-expression of LRP6 in hepatoma cells could partly mimic or counteract the anti-tumor properties of SAMC, respectively. administration of SAMC significantly suppressed the growth of Huh-7 xenograft/orthotopic HCC tumor without causing undesirable side effects. In addition, stable down-regulation of LRP6 in Huh-7 facilitated the anti-HCC effects of SAMC. In conclusion, LRP6 can be a potential therapeutic target of HCC. SAMC is a promising specific anti-tumor agent for treating HCC subtypes with Wnt activation at the hepatoma cell surface.

Authors : Xiao Jia, Xing Feiyue, Liu Yingxia, Lv Yi, Wang Xiaogang, Ling Ming-Tat, Gao Hao, Ouyang Songying, Yang Min, Zhu Jiang, Xia Yu, So Kwok-Fai, Tipoe George L,



(8) Synthesis, characterization and biological evaluation of Pd(ii), Cu(ii), Re(i) and Tc(i) thiazole-based complexes.[TOP]

Pubmed ID :30108972
Publication Date : //
A new thiazole-containing multidentate ligand 2-((2-phenylthiazol-4-yl)methylthio)ethanamine, L, was synthesized and used to prepare new complexes of the formula PdLCl (Pd-L), CuLCl (Cu-L) and -[Re/Tc(CO)(L)] (Re/Tc-L). The ligand L and the metal complexes were characterized spectroscopically. Furthermore, the structures of Re-L and Cu-L were elucidated by X-ray crystallography. Ligand L acts as a bidentate (N, S) chelator in Pd-L, as a bidentate (N, S) chelator in Cu-L and as a tridentate (N, S, N) chelator in Re-L. The radiotracer Tc-L was synthesized in high yield and characterised by HPLC comparison with the Re-L analog. The synthesized compounds were evaluated for their anti-inflammatory and cytotoxic properties. The compounds exhibited low anti-inflammatory activity with Pd-L showing the highest activity among them. The cytotoxic activity of the ligand and the complexes against several human cancer cell lines (cervical adenocarcinoma HeLa, colorectal adenocarcinoma LS-174T, lung adenocarcinoma A549, breast adenocarcinoma MDA-MB-231 and normal human lung fibroblast cell line MRC-5) was examined using the MTT assay. The complex Cu-L exhibited the highest cytotoxicity and the complex Pd-L showed the best tumor selectivity. The changes in the cell cycle phase distribution were determined by flow cytometry and it was found that ligand L shows the highest apoptotic activity. The biodistribution studies of Tc-L in mice showed fast tissue clearance. Of all the thiazole-containing compounds, the palladium complex appears to be more promising for future efforts.

Authors : Mašković Jelena M, Hatzidimitriou Antonios, Damjanović Ana, Stanojković Tatjana P, Trifunović Srećko R, Geronikaki Athina A, Papagiannopoulou Dionysia,



(9) Design, synthesis and biological evaluation of 3',4',5'-trimethoxy flavonoid benzimidazole derivatives as potential anti-tumor agents.[TOP]

Pubmed ID :30108924
Publication Date : //
A series of 3',4',5'-trimethoxy flavonoids with benzimidazole linked by different chain alkanes have been designed and synthesized. The potential activity of these compounds as anti-tumor agents was evaluated by cytotoxicity assay in MGC-803 (human gastric cancer), MCF-7 (human breast cancer), HepG-2 (human hepatoma) and MFC (mouse gastric cancer) tumor cell lines. Among them, compound 7-(3-(2-chloro-1-benzo[]imidazol-1-yl)propoxy)-2-(3,4,5-trimethoxyphenyl)-4-chromen-4-one displayed the most potent antiproliferative activity, with IC values of 20.47 ± 2.07, 43.42 ± 3.56, 35.45 ± 2.03 μM and 23.47 ± 3.59 μM, respectively. The flow cytometry (FCM) results showed that compound caused the cell cycle to be arrested in G1 phase and induced apoptosis of MFC cells in a dose-dependent manner. In addition, compound exhibited a significant inhibitory effect on tumor growth . All the results outlined the great potential of compound for further exploitation as anti-tumor agent.

Authors : Wang Zhe, Deng Xiangping, Xiong Runde, Xiong Shujuan, Liu Juan, Cao Xuan, Lei Xiaoyong, Chen Yanming, Zheng Xing, Tang Guotao,



(10) Soluble endoglin regulates expression of angiogenesis-related proteins and induction of arteriovenous malformations in a mouse model of hereditary hemorrhagic telangiectasia.[TOP]

Pubmed ID :30108051
Publication Date : //
Endoglin is a transmembrane glycoprotein expressed in vascular endothelium that plays a key role in angiogenesis. Mutations in the endoglin gene (ENG) cause Hereditary Hemorrhagic Telangiectasia type 1 (HHT1), characterized by arteriovenous malformations (AVMs) in different organs. These vascular lesions derive from abnormal processes of angiogenesis where aberrant vascular remodeling leads to focal loss of capillaries. Current treatments for HHT1 include anti-angiogenic therapies. Interestingly, a circulating form of endoglin (also known as soluble endoglin, sEng), proteolytically released from the membrane-bound protein and displaying anti-angiogenic activity, has been described in several endothelial-related pathological conditions. Using human and mouse endothelial cells, we find that sEng downregulates several pro-angiogenic and pro-migratory proteins involved in angiogenesis. However, this effect is much reduced in endothelial cells that lack endogenous transmembrane endoglin, suggesting that the anti-angiogenic activity of sEng is dependent on the presence of endogenous transmembrane endoglin protein. In fact, sEng partially restores the phenotype of endoglin-silenced endothelial cells back to that of normal endothelial cells. Moreover, using an established neonatal retinal model of HHT1 with depleted endoglin in the vascular endothelium, sEng treatment decreases the number of AVMs and has a normalizing effect on the vascular phenotype with respect to vessel branching, vascular density and migration of the vascular plexus towards the retinal periphery. Taken together these data show that circulating sEng can influence vascular development and AVMs by modulating angiogenesis and that its effect on endothelial cells depends on expression of endogenous endoglin.

Authors : Gallardo-Vara Eunate, Tual-Chalot Simon, Botella Luisa M, Arthur Helen M, Bernabeu Carmelo,