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#36484981   2022/12/09 To Up

Taurine Improves Sperm Mitochondrial Indices, Blunts Oxidative Stress Parameters, and Enhances Steroidogenesis and Kinematics of Sperm in Lead-Exposed Mice.

Lead (Pb) is a highly toxic heavy metal. Pb exposure could adversely affect many organs, including the male reproductive system. Oxidative stress and mitochondrial impairment play a fundamental role in the pathogenesis of Pb-induced male reproductive system injury. Taurine (TAU) is abundantly found in mammalian bodies. The positive effects of TAU on oxidative stress biomarkers and mitochondrial function have been reported. The current study evaluated the effects of TAU on Pb-induced reproductive toxicity. Mice received Pb (20 mg/kg/day; gavage, 35 consecutive days). Then, sperm indices (quality and quantity) together with sperm kinetics, sperm mitochondrial parameters, testicular and sperm oxidative stress biomarkers, testis and plasma testosterone levels, and the expression of genes involved in the steroidogenesis process have been evaluated. Pb caused significant histopathological alterations and oxidative stress in male mice's reproductive system and sperm. Moreover, significant mitochondrial function impairment was evident in sperm isolated from Pb-treated mice. Pb exposure also suppressed the expression of StAR, 17β-HSD, CYP11A, and 3β-HSD genes in the male gonad. It was found that TAU (500 and 1000 mg/kg) significantly improved oxidative stress biomarkers in both male gonads and gametes of Pb-treated mice. TAU also significantly restored sperm mitochondrial function and kinetics. The expression of genes involved in steroidogenesis was also higher in TAU-treated animals. These data suggest TAU as an effective agent against Pb-induced reproductive toxicity. The effects of TAU on oxidative stress markers, mitochondrial function, and the steroidogenesis process seem to play a fundamental role in its protective properties. Further studies are warranted to detect the precise protective effects of this amino acid in the reproductive system. Lead (Pb) is a toxic element that adversely affects the male reproductive system. Mitochondrial impairment and oxidative stress have a crucial role in the Pb-induced reproductive toxicity. Taurine (TAU) could considerably improve the reproductive toxicity induced by Pb via enhancing mitochondrial function and mitigating oxidative stress indices. ΔΨ, mitochondrial membrane potential; ATP, adenosine triphosphate.
Mohammad Mehdi Ommati, Samira Sabouri, Socorro Retana-Marquez, Hassan Nategh Ahmadi, Abdollah Arjmand, Sepideh Alidaee, Sahra Mazloomi, Alireza Akhlagh, Narges Abdoli, Hossein Niknahad, Akram Jamshidzadeh, Yanqin Ma, Negar Azarpira, Yaser Asefi, Reza Heidari

2147 related Products with: Taurine Improves Sperm Mitochondrial Indices, Blunts Oxidative Stress Parameters, and Enhances Steroidogenesis and Kinematics of Sperm in Lead-Exposed Mice.

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#36484970   2022/12/09 To Up

Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.

The altered expression of microRNA (miRNA) has been implicated in glioma. Here, the current study aimed to clarify the oncogenic effects of miR-19b-3p on cellular processes of glioma and to elucidate the underlying mechanism associated with SOCS3 and the JAK-STAT signaling pathway. Differentially expressed genes related to glioma were initially identified via microarray analysis. Twenty-five glioma patients were selected for clinical data collection, while additional 12 patients with traumatic brain injuries were selected as controls. Cell senescence was assessed by β-galactosidase staining, proliferation by MTT assay and apoptosis by flow cytometry following gain- and/or loss-of-function of miR-19b-3p or SOCS3. Glioma xenograft mouse model was developed through subcutaneous injection to nude mice to provide evidence in vivo. The glioma patients exhibited overexpressed miR-19b-3p and poorly-expressed SOCS3. SOCS3 was identified as a target gene of miR-19b-3p through dual-luciferase reporter gene assay. miR-19b-3p repressed SOCS3 expression and activated the JAK-STAT signaling pathway. Furthermore, miR-19b-3p inhibition promoted apoptosis and senescence, and suppressed cell proliferation through inactivation of the JAK-STAT signaling pathway and up-regulation of SOCS3. The reported regulatory axis was validated in nude mice as evidenced by suppressed tumor growth. Taken together, this study demonstrates that miR-19b-3p facilitates glioma progression via activation of the JAK-STAT signaling pathway by targeting SOCS3, highlighting a novel therapeutic target for glioma treatment.
Tao Li, Hong Ge, Qingyan Yang, Junmei Wang, Qian Yin, Hongbin Wang, Gaolei Hou

2857 related Products with: Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.

2 Pieces/Box2 mg2 Pieces/Box2 Pieces/Box5 mg8 inhibitors100ug2 Pieces/Box1 Set1 Set1 Set 100 UG

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#36484954   2022/12/09 To Up

Fear stress promotes glioma progression through inhibition of ferroptosis by enhancing FSP1 stability.

Patients diagnosed with cancer often suffer from emotional stressors, such as anxiety, depression, and fear of death. However, whether fear stress could influence the glioma progression is still unclear.
Chaojie Bu, Sen Hu, Jinliang Yu, Nianxuan Li, Jianjun Gu, Zhiyuan Sheng, Zhaoyue Yan, Xingyao Bu

1253 related Products with: Fear stress promotes glioma progression through inhibition of ferroptosis by enhancing FSP1 stability.

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#36484925   2022/12/09 To Up

S100A6 Activates Kupffer Cells via the p-P38 and p-JNK Pathways to Induce Inflammation, Mononuclear/macrophage Infiltration Sterile Liver Injury in Mice.

Noninfectious liver injury, including the effects of chemical material, drugs and diet, is a major cause of liver diseases worldwide. In chemical and drugs-induced liver injury, innate inflammatory responses are mediated by extracellular danger signals. The S100 protein can act as danger signals, which can promote the migration and chemotaxis of immune cells, promote the release of various inflammatory cytokines, and regulate the body's inflammatory and immune responses. However, the role of S100A6 in inflammatory response in chemical and drugs-induced sterile liver injury remains unclear. We constructed the model of sterile liver injury induced by carbon tetrachloride (CCl)/Paracetamol (APAP) and performed RNA sequencing (RNA-seq) on the liver tissues after injury (days 2 and 5). We analyzed inflammatory protein secretion in the liver tissue supernatant by enzyme-linked immunosorbent assay (ELISA), determined the inflammation response by bioinformatic analysis during sterile liver injury, and assessed mononuclear/macrophage infiltration by immunohistochemistry and flow cytometry. Immunohistochemistry was used to analyze the location of S100A6. We conducted inflammatory factor expression analysis and molecular mechanistic studies in Kupffer cells (KCs) induced by S100A6 using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), ELISA, and western blot in vitro experiments. We performed chemokine CCL2 expression analysis and molecular mechanism studies using the same method. We used a Transwell assay to show the infiltration of mononuclear/macrophage. We here observed that aggravated inflammatory response was shown in CCl and APAP-administrated mice, as evidenced by enhanced production of inflammatory cytokines (TNF-α, IL-1β), and elevated mononuclear/macrophage infiltration and activation of immunity. The expression of S100A6 was significantly increased on day 2 after sterile liver injury, which is primarily produced by injured liver cells. Mechanistic studies established that S100A6 activates Kupffer cells (KCs) via the p-P38, p-JNK and P65 pathways to induce inflammation in vitro. Furthermore, TNF-α can stimulate liver cells via the p-P38 and p-JNK pathways to produce CCL2 and promote the infiltration of mononuclear/macrophage. In summary, we showed that S100A6 plays an important role in regulating inflammation, thus influencing sterile liver injury. Our findings provide novel evidence that S100A6 can as a danger signal that contributes to pro-inflammatory activation through p-P38 and p-JNK pathways in CCl and APAP-induced sterile liver injury in mice. In addition, the inflammatory factor TNF-α induces a large amount of CCL2 production in normal liver cells surrounding the injured area through a paracrine action, which is chemotactic for blood mononuclear/macrophage infiltration.
He Tong, Li Wang, Kefan Zhang, Jing Shi, Yongshuai Wu, Yulong Bao, Changshan Wang

1600 related Products with: S100A6 Activates Kupffer Cells via the p-P38 and p-JNK Pathways to Induce Inflammation, Mononuclear/macrophage Infiltration Sterile Liver Injury in Mice.

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#36484879   2022/12/09 To Up

Benzophenones alter autophagy and ER stress gene expression in pancreatic beta cells in vitro.

Benzophenones (BPs) are endocrine disruptors frequently used in sunscreens and food packaging as UV blockers. Our goal was to assess the effect of benzophenone 2 (BP2) and 3 (BP3) on gene expression related to autophagy process and ER stress response in pancreatic beta cells. To that end, the mouse pancreatic beta cell line MIN6B1 was treated with 10 µM BP2 or BP3 in the presence or absence of the autophagy-inhibitor chloroquine (CQ, 10 µM) or the autophagy-inducer rapamycin (RAPA, 50 nM) during 24 h. BP3 inhibited the expression of the autophagic gene Ulk1, and additional effects were uncovered when autophagy was modified by CQ and RAPA. BP3 counteracted CQ-induced Lamp2 expression but did not compensate CQ-induced Sqstm1/p62 gene transcription, neither BP2. Nevertheless, the BPs did not alter the autophagic flux. In relation to ER stress, BP3 inhibited unspliced and spliced Xbp1 mRNA levels in the presence or absence of CQ, totally counteracted CQ-induced Chop gene expression, and partially reverted CQ-induced Grp78/Bip mRNA levels, while BP2 also partially inhibited Grp78/Bip mRNA induction by CQ. In conclusion, BPs, principally BP3, affect cellular adaptive responses related to autophagy, lysosomal biogenesis, and ER stress in pancreatic beta cells, indicating that BP exposure could lead to beta cell dysfunction.
Florencia Szulak, Luz Etcheverry Boneo, Damasia Becu-Villalobos, Marina Olga Fernandez, Eleonora Sorianello

1329 related Products with: Benzophenones alter autophagy and ER stress gene expression in pancreatic beta cells in vitro.

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#36484857   2022/12/09 To Up

Development of minimally invasive cancer immunotherapy using anti-disialoganglioside GD2 antibody-producing mesenchymal stem cells for a neuroblastoma mouse model.

Mouse IgG anti-disialoganglioside GD2 antibody-secreting mouse mesenchymal stem cells (anti-GD2-MSCs) were developed, and their anti-tumor effects were validated in an in vivo neuroblastoma mouse model.
Kosuke Kambe, Masafumi Iguchi, Mayumi Higashi, Shigeki Yagyu, Shigehisa Fumino, Tsunao Kishida, Osam Mazda, Tatsuro Tajiri

1707 related Products with: Development of minimally invasive cancer immunotherapy using anti-disialoganglioside GD2 antibody-producing mesenchymal stem cells for a neuroblastoma mouse model.

25 µg25 µg100ul0.25 mg100 TESTS100ul0.2 mg1 ml0.2 mg100ug100ug100ul

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#36484822   2022/12/09 To Up

Possible transfer of lncRNA H19-derived miRNA miR-675-3p to adjacent H19-non-expressing trophoblast cells in near-term mouse placenta.

LncRNA H19 serves as a regulatory RNA in mouse placental development. However, there is little information available on the in situ expression of H19 in the late-gestation mouse placenta. In this study, we performed quantitative polymerase chain reaction (qPCR) and in situ hybridization (ISH) analyses of lncRNA H19 and its exon 1-derived miRNA miR-675-3p to identify cell types expressing these non-coding RNAs in the mouse placenta during mid-to-late gestation. By qPCR analysis, we confirmed that H19 was highly expressed during mid-to-late gestation (E10.5-E18.5) and that H19-derived miRNA miR-675-3p was remarkably upregulated in the E18.5 placenta. ISH analysis revealed trophoblast cell type-specific expression of lncRNA H19 and miR-675-3p during later stages of gestation. In the junctional zone and decidua of late-gestation placenta, H19 was expressed in trophoblast giant cells and glycogen trophoblast cells; however, H19 was absent in spongiotrophoblast cells. In the labyrinth and chorionic plate, H19 was present in sinusoidal mononuclear trophoblast giant cells, fetal vascular endothelial cells, and basal chorionic trophoblast cells, but not in syncytiotrophoblasts. As expected, these lncRNA H19-expressing cells exhibited miR-675-3p in the E18.5 placenta. Intriguingly, miR-675-3p was also present in H19-negative spongiotrophoblast cells and syncytiotrophoblasts, implying the possible transfer of miR-675-3p from H19-exprssing cells to adjacent H19-non-expressing trophoblast cells. These findings suggest that the mouse placenta expresses lncRNA H19 in a trophoblast cell type-specific fashion during later stages of gestation.
Banyar Than Naing, Takami Takizawa, Takanobu Sakurai, Chaw Kyi-Tha-Thu, Toshihiro Takizawa

1962 related Products with: Possible transfer of lncRNA H19-derived miRNA miR-675-3p to adjacent H19-non-expressing trophoblast cells in near-term mouse placenta.

100 μg1.00 flask100 μg2 ml96 wells (1 kit)0.2 mg100 μg1.00 flask100 μg100 μg100 μg

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#36484786   2022/12/09 To Up

Intermittent theta burst transcranial magnetic stimulation induces hippocampal mossy fiber plasticity in male but not female mice.

Transcranial magnetic stimulation (TMS) induces electric fields that depolarize or hyperpolarize neurons. Intermittent theta burst stimulation (iTBS), a patterned form of TMS that is delivered at the theta frequency (~5 Hz), induces neuroplasticity in the hippocampus, a brain region that is implicated in memory and learning. One form of plasticity that is unique to the hippocampus is adult neurogenesis, however little is known about whether TMS, or iTBS in particular, affects newborn neurons. Here we therefore applied repeated sessions of iTBS to male and female mice and measured the extent of adult neurogenesis and the morphological features of immature neurons. We found that repeated sessions of iTBS did not significantly increase the amount of neurogenesis or affect the gross dendritic morphology of new neurons, and there were no sex differences in neurogenesis rates or aspects of afferent morphology. In contrast, efferent properties of newborn neurons varied as a function of sex and stimulation. Chronic iTBS increased the size of mossy fiber terminals, which synapse onto CA3 pyramidal neurons, but only in males. iTBS also increased the number of terminal-associated filopodia, putative synapses onto inhibitory interneurons, but only in male mice. This efferent plasticity could be result from a general trophic effect or it could reflect accelerated maturation of immature neurons. Given the important role of mossy fiber synapses in hippocampal learning, our results identify a neurobiological effect of iTBS that might be associated with sex-specific changes in cognition.
Tian Rui Zhang, Baran Askari, Aydan Kesici, Evelyn Guilherme, Fidel Vila-Rodriguez, Jason S Snyder

1739 related Products with: Intermittent theta burst transcranial magnetic stimulation induces hippocampal mossy fiber plasticity in male but not female mice.

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#36484784   2022/12/09 To Up

Recognition of Core-Fucosylated Glycopeptides Based on the Y1+Fuc/Y1 Ratio in Low-Energy HCD Spectra.

Accurate identification of core fucosylation on -glycopeptides remains challenging due to fucose migration during mass spectrometry analysis. Here, we introduce a simple and straightforward method for core-fucosylated glycopeptide recognition based on the relative intensities of Y1+Fuc ions compared with their corresponding Y1 ions (labeled as Y1+Fuc/Y1 or simply Y1F/Y1 ratio > 0.1) in low-energy HCD-based spectra. The method was first developed by systematically evaluating the influence of fucose migration on the Y1F ion from antenna fucoses based on the distribution of the Y1F/Y1 ratios in the MS/MS spectra of antenna-fucosylated glycopeptides from Fut8 mouse brain. The feasibility of the method was then confirmed by using two standard glycoproteins, comparison with glycopeptides in Fut8 mouse brain with/without in silico core-fucosylation removal, and Y1F/Y1 ratio alterations under a lower HCD energy. This method will be applicable to the manual interpretation and software-based high-throughput analysis of core-fucosylated glycopeptides.
Zexuan Chen, Jiechen Shen, Wenbo Dong, Pengfei Li, Miaomiao Xin, Didi Liu, Li Jia, Bojing Zhu, Wenzhe Li, Shisheng Sun

2169 related Products with: Recognition of Core-Fucosylated Glycopeptides Based on the Y1+Fuc/Y1 Ratio in Low-Energy HCD Spectra.

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