38 results on '"Zhao, Jingsong"'
Search Results
2. The impact of digital carbon communication on market response to carbon disclosure: The moderating effects of external supervision
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Zhu, Jing, Zhang, Chen, Zhao, Jingsong, and Sun, Jiaojiao
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- 2024
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3. Copper exposure induces trophoblast cell cuproptosis by up-regulating lnc-HZ11
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Zheng, Zhaodian, Fang, Jing, Shen, Yanqiu, Mi, Chenyang, Xu, Zhongyan, Zhao, Jingsong, Chen, Weina, Han, Ruining, Lei, Qiong, and Zhang, Huidong
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- 2024
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4. BaP/BPDE suppresses human trophoblast cell migration/invasion and induces unexplained miscarriage by up-regulating a novel lnc-HZ11 in extracellular vesicles: An intercellular study
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Mi, Chenyang, Chen, Weina, Zhang, Ying, Yang, Yang, Zhao, Jingsong, Xu, Zhongyan, Sun, Yi, Fan, Qigang, Huang, Wenxin, Guo, Geng, and Zhang, Huidong
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- 2024
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5. Environmental copper exposure, placental cuproptosis, and miscarriage
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Zhao, Jingsong, Xu, Zhongyan, Wang, Xiaoqing, Wan, Shukun, Chen, Weina, Huang, Wenxin, Wang, Manli, Wang, Rong, and Zhang, Huidong
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- 2024
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6. Hypoxia causes trophoblast cell ferroptosis to induce miscarriage through lnc-HZ06/HIF1α-SUMO/NCOA4 axis
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Tian, Peng, Xu, Zhongyan, Guo, Jiarong, Zhao, Jingsong, Chen, Weina, Huang, Wenxin, Wang, Manli, Mi, Chenyang, Zhang, Ying, Yang, Yang, and Zhang, Huidong
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- 2024
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7. BaP/BPDE suppressed endothelial cell angiogenesis to induce miscarriage by promoting MARCHF1/GPX4-mediated ferroptosis
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Zhang, Ying, Yang, Yang, Chen, Weina, Mi, Chenyang, Xu, Xiaole, Shen, Yanqiu, Zheng, Zhaodian, Xu, Zhongyan, Zhao, Jingsong, Wan, Shukun, Wang, Xiaoqing, and Zhang, Huidong
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- 2023
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8. Defective Homologous Recombination Repair By Up‐Regulating Lnc‐HZ10/Ahr Loop in Human Trophoblast Cells Induced Miscarriage.
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Chen, Weina, Mi, Chenyang, Zhang, Ying, Yang, Yang, Huang, Wenxin, Xu, Zhongyan, Zhao, Jingsong, Wang, Rong, Wang, Manli, Wan, Shukun, Wang, Xiaoqing, and Zhang, Huidong
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HOMOLOGOUS recombination ,TROPHOBLAST ,MISCARRIAGE ,ARYL hydrocarbon receptors ,RECURRENT miscarriage ,BRCA genes - Abstract
Human trophoblast cells are crucial for healthy pregnancy. However, whether the defective homologous recombination (HR) repair of dsDNA break (DSB) in trophoblast cells may induce miscarriage is completely unknown. Moreover, the abundance of BRCA1 (a crucial protein for HR repair), its recruitment to DSB foci, and its epigenetic regulatory mechanisms, are also fully unexplored. In this work, it is identified that a novel lnc‐HZ10, which is highly experssed in villous tissues of recurrent miscarriage (RM) vs their healthy control group, suppresses HR repair of DSB in trophoblast cell. Lnc‐HZ10 and AhR (aryl hydrocarbon receptor) form a positive feedback loop. AhR acts as a transcription factor to promote lnc‐HZ10 transcription. Meanwhile, lnc‐HZ10 also increases AhR levels by suppressing its CUL4B‐mediated ubiquitination degradation. Subsequently, AhR suppresses BRCA1 transcription; and lnc‐HZ10 (mainly 1‐447 nt) interacts with γ‐H2AX; and thus, impairs its interactions with BRCA1. BPDE exposure may trigger this loop to suppress HR repair in trophoblast cells, possibly inducing miscarriage. Knockdown of murine Ahr efficiently recovers HR repair in placental tissues and alleviates miscarriage in a mouse miscarriage model. Therefore, it is suggested that AhR/lnc‐HZ10/BRCA1 axis may be a promising target for alleviation of unexplained miscarriage. [ABSTRACT FROM AUTHOR]
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- 2024
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9. Exposure to high dose of polystyrene nanoplastics causes trophoblast cell apoptosis and induces miscarriage.
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Wan, Shukun, Wang, Xiaoqing, Chen, Weina, Wang, Manli, Zhao, Jingsong, Xu, Zhongyan, Wang, Rong, Mi, Chenyang, Zheng, Zhaodian, and Zhang, Huidong
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TROPHOBLAST ,MISCARRIAGE ,EXPOSURE dose ,HUMAN reproduction ,RECURRENT miscarriage ,POLYSTYRENE - Abstract
Background: With rapid increase in the global use of various plastics, microplastics (MPs) and nanoplastics (NPs) pollution and their adverse health effects have attracted global attention. MPs have been detected out in human body and both MPs and NPs showed female reproductive toxicological effects in animal models. Miscarriage (abnormal early embryo loss), accounting for 15-25% pregnant women worldwide, greatly harms human reproduction. However, the adverse effects of NPs on miscarriage have never been explored. Results: In this study, we identified that polystyrene (PS) plastics particles were present in women villous tissues. Their levels were higher in villous tissues of unexplained recurrent miscarriage (RM) patients vs. healthy control (HC) group. Furthermore, mouse assays further confirmed that exposure to polystyrene nanoplastics (PS-NPs, 50 nm in diameter, 50 or 100 mg/kg) indeed induced miscarriage. In mechanism, PS-NPs exposure (50, 100, 150, or 200 µg/mL) increased oxidative stress, decreased mitochondrial membrane potential, and increased apoptosis in human trophoblast cells by activating Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3 signaling through mitochondrial pathway. The alteration in this signaling was consistent in placental tissues of PS-NPs-exposed mouse model and in villous tissues of unexplained RM patients. Supplement with Bcl-2 could efficiently suppress apoptosis in PS-NPs-exposed trophoblast cells and reduce apoptosis and alleviate miscarriage in PS-NPs-exposed pregnant mouse model. Conclusions: Exposure to PS-NPs activated Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3, leading to excessive apoptosis in human trophoblast cells and in mice placental tissues, further inducing miscarriage. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Cancer communication research in the era of genomics and precision medicine: a scoping review
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Kaphingst, Kimberly A., Peterson, Emily, Zhao, Jingsong, Gaysynsky, Anna, Elrick, Ashley, Hong, Soo Jung, Krakow, Melinda, Pokharel, Manusheela, Ratcliff, Chelsea L., Klein, William M. P., Khoury, Muin J., and Chou, Wen-Ying Sylvia
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- 2019
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11. Substantial N2O emission during the initial period of the wheat season due to the conversion of winter-flooded paddy to rice-wheat rotation
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Zhou, Wei, Lin, Shan, Wu, Lei, Zhao, Jingsong, Wang, Milan, Zhu, Bo, Mo, Yongliang, Hu, Ronggui, Chadwick, Dave, and Shaaban, Muhammad
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- 2017
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12. Mitogenic Influence of Human R-Spondin1 on the Intestinal Epithelium
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Kim, Kyung-Ah, Kakitani, Makoto, Zhao, Jingsong, Oshima, Takeshi, Tang, Tom, Binnerts, Minke, Liu, Yi, Boyle, Bryan, Park, Emily, Emtage, Peter, Funk, Walter D., and Tomizuka, Kazuma
- Published
- 2005
13. Maritime collision and liability
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Zhao, Jingsong
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623.8 ,Marine engineering & offshore engineering - Abstract
Collision prevention and liability is analyzed from both the legal and the technical aspects. The time when the Rules begin to apply is analyzed first, with the conclusion that the Collision Regulations begin to apply when two vessels are approaching so as to involve risk of collision, the risk of collision will exist immediately. The risk of collision within the Rules consists of three elements, namely small DCPA, closing enough and possibility of unco-ordinated action. Rule 7 is not good enough to define the risk of collision. Furthermore, the legal interpretation of the Rule 17(a)(i) and (ii) is discussed, especially the legal meaning of course and speed and the special circumstances when the stand-on vessel is released from her duty to keep course and speed although she alterates them. Some other comments are made on whether the Rule 17(a)(ii) is an option or an obligation and other aspects of the Rules. This study has used data obtained at sea from particular cases of behaviour as it happened. Decision making simulation models are developed with fuzzy programming methods. The uncertainty and uncoordination of mariner's behaviour is examined with such models. Finally, an automatic collision avoidance decision making system (ACAS) is developed with fuzzy sets and neural networks, whose application to collision liability division is also discussed.
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- 1996
14. Your Family Connects: A Theory-Based Intervention to Encourage Communication about Possible Inherited Cancer Risk among Ovarian Cancer Survivors and Close Relatives.
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Zhao, Jingsong, McBride, Colleen M., Campbell, Gavin P., Pentz, Rebecca D., Escoffery, Cam, Konomos, Michael, Bellcross, Cecelia, Ward, Kevin, Shepperd, James R., and Guan, Yue
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DISEASE risk factors , *OVARIAN cancer , *CANCER survivors , *INTERDEPENDENCE theory , *FAMILY communication , *TUMOR markers - Abstract
Introduction: Encouraging family communication about possible genetic risk has become among the most important avenues for achieving the full potential of genomic discovery for primary and secondary prevention. Yet, effective family-wide risk communication (i.e., conveying genetic risk status and its meaning for other family members) remains a critical gap in the field. We aim to describe the iterative process of developing a scalable population-based communication outreach intervention, Your Family Connects, to reach ovarian cancer survivors and close relatives to communicate the potential for inherited risk and to consider genetic counseling. Methods: Relational-level theories (e.g., interdependence theory) suggest that interventions to promote family cancer risk communication will be most effective if they consider the qualities of specific relationships and activate motives to preserve the relationship. Informed by these theories, we collaborated with 14 citizen scientists (survivors of ovarian cancer or relatives) and collected 261 surveys and 39 structured interviews over 12 weeks of citizen science activities in 2020. Results: The citizen science findings and consideration of relational-level theories informed the content and implementation of Your Family Connects (www.yourfamilyconnects.org). CS results showed survivors favor personal contact with close relatives, but relatives were open to alternative contact methods, such as through health professionals. Recognizing the need for varied approaches based on relationship dynamics, we implemented a relative contact menu to enable survivors identify at-risk relatives and provide multiple contact options (i.e., survivor contact, health professional contact, and delayed contact). In line with relational autonomy principles, we included pros and cons for each option, assisting survivors in choosing suitable contact methods for each relative. Discussion: Our developed intervention represents a novel application of relational-level theories and partnership with citizen scientists to expand genetic services reach to increase the likelihood for fair distribution of cancer genomic advances. The Your Family Connects intervention as part of a randomized trial in collaboration with the Georgia Cancer Registry compared with standard outreach. [ABSTRACT FROM AUTHOR]
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- 2023
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15. R-Spondin1 Protects Mice from Chemotherapy or Radiation-Induced Oral Mucositis through the Canonical Wnt/β-Catenin Pathway
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Zhao, Jingsong, Kim, Kyung-Ah, De Vera, Josephine, Palencia, Servando, Wagle, Marie, Abo, Arie, and Karin, Michael
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- 2009
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16. Preparation and characterization of Mo-15 Cu superfine powders by a gelatification-reduction process
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Song, Peng, Cheng, Jigui, Wan, Lei, Zhao, Jingsong, Wang, Yifang, and Cai, Yanbo
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- 2009
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17. TACE is required for fetal murine cardiac development and modeling
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Shi, Wei, Chen, Hui, Sun, Jianping, Buckley, Sue, Zhao, Jingsong, Anderson, Kathryn D., Williams, Roberta G., and Warburton, David
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Heart cells -- Research ,Tumor necrosis factor -- Physiological aspects ,Tumor necrosis factor -- Research ,Biological sciences - Abstract
Tumor necrosis factor-[alpha] converting enzyme (TACE) is a membrane-anchored, Zn-dependent metalloprotease, which belongs to the ADAM (a disintegrin and metalloprotease) family. TACE functions as a membrane sheddase to release the ectodomain portions of many transmembrane proteins, including the precursors of TNF[alpha] , TGF[alpha], several other cytokines, as well as the receptors for TNF[alpha], and neuregulin (ErbB4). Mice with [TACE.sup.[delta]Zn/[delta]Zn] null mutation die at birth with phenotypic changes, including failure of eyelid fusion, hair and skin defects, and abnormalities of lung development. Abnormal fetal heart development was not previously described. Herein, we report that [TACE.sup.[delta]Zn/[delta]Zn] null mutant mice by late gestation exhibit markedly enlarged fetal hearts with increased myocardial trabeculation and reduced cell compaction, mimicking the pathological changes of noncompaction of ventricular myocardium. In addition, larger cardiomyocyte cell size and increased cell proliferation were observed in ventricles of [TACE.sup.[delta]Zn/[delta]Zn] knockout mouse hearts. At the molecular level, reduced expression of epidermal growth factor receptor, attenuated protein cleavage of ErbB4, and changes in MAPK activation were also detected in [TACE.sup.[delta]Zn/[delta]Zn] knockout heart tissues. The data suggest that TACE-mediated cell surface protein ectodomain shedding plays an essential and a novel regulatory role during cardiac development and modeling. Keywords: TACE; Heart development; Cardiomyocyte
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- 2003
18. Applying citizen science to engage families affected by ovarian cancer in developing genetic service outreach strategies.
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McBride, Colleen M., Campbell, Gavin P., Zhao, Jingsong, Pentz, Rebecca D., Escoffery, Cam, Komonos, Michael, Cannova, Kelly, Byrne, Janice L. B., Paris, Nancy M., Shepperd, James R., and Guan, Yue
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OVARIAN cancer ,CITIZEN science ,INTERNET content ,SUPPORT groups ,ONLINE education ,ACQUISITION of data - Abstract
Citizen science (CS) approaches involving non-professional researchers (citizens) as research collaborators has been used infrequently in health promotion generally and specifically, in cancer prevention. Standardized CS approaches may be especially useful for developing communication interventions to encourage families to consider cancer genetic services. We engaged survivors of ovarian cancer and their close relatives as CS collaborators to collect and help interpret data to inform content for a website, printed invitation materials, and short-message reminders. We applied an implementation quality framework, and posed four research questions regarding the feasibility of CS: recruitment, data collection, data quality and evaluation of the experience. CS members were recruited through three networks: clinical sites, local and national cancer support organizations, and online ovarian cancer patient support groups. The professional research team operationalized theory-aligned CS tasks, five data collection options, question banks/scripts for creating surveys, structured interviews, online training and ongoing support from research coaches. 14 CS members agreed to the 12-week and 20-hour commitment for an honorarium. CS members opted to do both qualitative and quantitative assessments. CS members collected 261 surveys and 39 structured interviews. The largest number of surveys were collected for Task 1 (n = 102) to assess survivors' reactions to different possible options for motivating survivors to visit a study website; 77% of this data were complete (i.e., no missing values). Data collected for tasks 2, 3, 4, and 5 (e.g., assessment of survivors' and relatives' respective communication preferences) ranged from 10 to 58 surveys (80% to 84% completeness). All data were collected within the specified time frame. CSs reported 17 hours of work on average and regarded the experience positively. Our experience suggests that CS engagement is feasible, can yield comprehensive quantitative and qualitative data, and is achievable in a relatively a short timeline. [ABSTRACT FROM AUTHOR]
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- 2022
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19. Do Lung Remodeling, Repair, and Regeneration Recapitulate Respiratory Ontogeny?
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WARBURTON, DAVID, TEFFT, DENISE, MAILLEUX, ARNAUD, BELLUSCI, SAVERIO, THIERY, JEAN-PAUL, ZHAO, JINGSONG, BUCKLEY, SUE, SHI, WEI, and DRISCOLL, BARBARA
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- 2001
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20. Mechanism of Systemic Iron Regulation and Hematocrit Control By Hepcidin Peptidomimetics in Pre-Clinical Models
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Taranath, Roopa, Mattheakis, Larry, Zhao, Li, Lee, Larry, Tovera, James, Zhao, Jingsong, Cheng, Xiaoli, and Liu, David
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- 2020
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21. An allosteric antibody to the leptin receptor reduces body weight and reverses the diabetic phenotype in the Lep(ob) /Lep(ob) mouse.
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Bhaskar, Vinay, Goldfine, Ira D., Gerstner, Resi, Michelson, Kristen, Tran, Catarina, Nonet, Genevieve, Bohmann, David, Pongo, Elizabeth, Zhao, Jingsong, Horwitz, Arnold H., Takeuchi, Toshihiko, White, Mark, and Corbin, John A.
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LEPTIN receptors ,ALLOSTERIC regulation ,BODY weight ,NEUROPEPTIDE Y ,PROOPIOMELANOCORTIN ,HYPERPHAGIA ,BLOOD sugar ,LABORATORY mice - Abstract
Objective: Leptin (LEP) deficiency results in major metabolic perturbations, including obesity, dyslipidemia, and diabetes. Although LEP deficiency can be treated with daily injections of a recombinant LEP, generation of an antibody activating the LEP receptor (LEPR) that has both an intrinsically long half-life and low immunogenicity could be useful in the treatment of this condition.Methods: Phage display technology coupled with flow cytometry and cell-based in vitro assays were employed to identify an allosteric agonist of the mouse LEPR. LEP-deficient Lep(ob) /Lep(ob) mice were used to compare in vivo effects of LEP to antibody administration. To evaluate hypothalamic effects of treatment, changes in mRNA levels of neuropeptide Y and proopiomelanocortin were measured.Results: XPA.80.037 is a monoclonal antibody that demonstrates allosteric agonism of the mouse LEPR. Treatment of Lep(ob) /Lep(ob) mice with XPA.80.037 markedly reduced hyperphagia and body weight, normalized blood glucose and plasma insulin levels, and corrected dyslipidemia. These metabolic alterations correlated with changes in mRNA levels of neuropeptide Y and proopiomelanocortin, suggesting that XPA.80.037 had hypothalamic effects.Conclusions: Agonist allosteric monoclonal antibodies to the LEPR can correct metabolic effects associated with LEP deficiency in vivo and thereby have the potential to treat conditions of LEP deficiency. [ABSTRACT FROM AUTHOR]- Published
- 2016
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22. BPDE induces human trophoblast cell ferroptosis by up-regulating iron metabolism and promoting GPX4 proteasomal degradation.
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Tian, Peng, Xu, Zhongyan, Guo, Jiarong, Zhao, Jingsong, Wang, Rong, Chen, Weina, Yang, Yang, Huang, Wenxin, Mi, Chenyang, and Zhang, Huidong
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IRON metabolism ,TROPHOBLAST ,APOPTOSIS ,REACTIVE oxygen species ,PROTEOLYSIS ,LIPID metabolism ,CELL migration ,CELL migration inhibition - Abstract
Human trophoblast cells play important role in embryo-fetal development. However, trophoblast cells are sensitive to environmental carcinogens. Recently, we have discovered that BPDE inhibits trophoblast cell migration, invasion and proliferation, and also increases trophoblast cell apoptosis. Ferroptosis is a newly identified iron-dependent non-apoptotic programmed cell death. Whether BPDE might induce trophoblast cell ferroptosis is completely unknown. In this work, we have discovered that ferroptosis does occur in BPDE-treated human trophoblast cells. Iron metabolism up-regulates intracellular free Fe
2+ level, produces excessive ROS (reactive oxygen species), and accelerates lipid peroxidation. GPX4 efficiently eliminates ROS and inhibits lipid peroxidation. Thus, ferroptosis is well suppressed due to the balance of these two pathways in healthy trophoblast cells. However, BPDE exposure could promote iron metabolism, increase intracellular free Fe2+ level, produce excessive ROS, and result in lipid peroxidation. Meanwhile, BPDE also down-regulates GPX4 expression level by promoting its proteasomal degradation, which eventually produces excessive ROS and induces lipid peroxidation. Thus, BPDE exposure induces trophoblast cell ferroptosis by unbalancing these two pathways, providing new insight in understanding BPDE-induced dysfunctions of human trophoblast cells. • BPDE exposure induces human trophoblast cell ferroptosis. • BPDE exposure increases intracellular free Fe2+ level and ROS level. • BPDE promotes GPX4 proteasomal degradation and reduces its protein level. • BPDE produces excessive ROS and induces lipid peroxidation. [ABSTRACT FROM AUTHOR]- Published
- 2021
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23. R-spondin1, A Novel Intestinotrophic Mitogen, Ameliorates Experimental Colitis in Mice.
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Zhao, Jingsong, de Vera, Josephine, Narushima, Seiko, Beck, Eric X., Palencia, Servando, Shinkawa, Pauline, Kim, Kyung–Ah, Liu, Yi, Levy, Michael D., Berg, Daniel J., Abo, Arie, and Funk, Walter D.
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MITOGENS ,INFLAMMATORY bowel diseases ,COLITIS ,GRANULOCYTE-macrophage colony-stimulating factor - Abstract
Background & Aims: R-spondin 1 (Rspo1) is a novel epithelial mitogen that stimulates the growth of mucosa in both the small and large intestine. Methods: We investigated the therapeutic potential of Rspo1 in ameliorating experimental colitis induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) as well as nonsteroidal anti-inflammatory drug–induced colitis in interleukin (IL)-10–decifient mice. Results: Therapeutic administration of recombinant Rspo1 protein reduced the loss of body weight, diarrhea, and rectal bleeding in a mouse model of acute or chronic DSS-induced colitis. Histologic evaluation revealed that Rspo1 improved mucosal integrity in both villus and/or crypt compartments in the small intestine and colon by stimulating crypt cell growth and mucosal regeneration in DSS-treated mice. Moreover, Rspo1 significantly reduced DSS-induced myeloperoxidase activity and inhibited the overproduction of proinflammatory cytokines, including tumor necrosis factor-α, IL-1α, IL-6, interferon-γ, and granulocyte-macrophage colony–stimulating factor, in mouse intestinal tissue, indicating that Rspo1 may reduce DSS-induced inflammation by preserving the mucosal barrier function. Likewise, Rspo1 therapy also alleviated TNBS–induced interstitial inflammation and mucosal erosion in the mouse colon. Furthermore, Rspo1 substantially decreased the histopathologic severity of chronic enterocolitis by repairing crypt epithelium and simultaneously suppressing inflammatory infiltration in piroxicam-exposed IL-10
−/− mice. Endogenous Rspo1 protein was localized to villus epithelium and crypt Paneth cells in mouse small intestine. Conclusions: Our results show that Rspo1 may be clinically useful in the therapeutic treatment of inflammatory bowel disease by stimulating crypt cell growth, accelerating mucosal regeneration, and restoring intestinal architecture. [Copyright &y& Elsevier]- Published
- 2007
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24. Adenovirus-mediated decorin gene transfer prevents TGF-beta-induced inhibition of lung...
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Zhao, Jingsong and Sime, Patricia J.
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TRANSFORMING growth factors , *MORPHOGENESIS - Abstract
Deals with a study which used decorin to antagonize exogenous tumor growth factor (TGF)-beta-mediated inhibition of lung morphogenesis and cytodifferentiation in a model of embryonic mouse lung morphogenesis ex vivo. Effects of decorin on the TGF-beta-mediated inhibition of embryonic lung development; How intratracheal microinjection of adenovirus carrying human decorin cDNA (AdDcn) prevents TGF-beta-mediated inhibition of embryonic lung branching.
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- 1999
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25. Molecular embryology of the lung: then, now, and in the future.
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Warburton, David and Zhao, Jingsong
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LUNGS , *EMBRYOLOGY , *MORPHOGENESIS , *MOLECULES - Abstract
Presents information on a study which examined the molecular embryology of the lung. Genetics of tracheal branching morphogenesis in Drosophila; Pattern formation in the anterior foregut and the morphogenetic function of NKX2.1, a thyroid transcription factor-1; How transcription factors interact in regulatory networks to determine lung epithelial cell fate; Integration of signaling systems in lung morphogenesis.
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- 1999
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26. Potent Anti-Cancer Activity of Anti-NTB-a Monoclonal Antibodies in Preclinical Leukemia and Lymphoma Models
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Korver, Wouter, Zhao, Xiaoxian, Singh, Shweta, Pardoux, Cecile, Barman, Ishita, Aguilar, Gerard, Zhao, Jingsong, Hsi, Eric, and Abo, Arie
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- 2008
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27. CLL-1, a Receptor Expressed on Myeloid Leukemic Stem Cells, Is a Potential Target for Immunotherapy of AML
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Korver, Wouter, Zhao, Xiaoxian, Singh, Shweta, Pardoux, Cecile, Zhao, Jingsong, Sen, Siddhartha, Guzman, Monica L., Jordan, Craig T., Hsi, Eric D, and Abo, Arie
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- 2008
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28. rNAPc2, a Novel Inhibitor of Tissue Factor/Factor VIIa Complex, Inhibits Tumor Growth and Metastasis in Mouse Models of Colorectal Cancer.
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Zhao, Jingsong, Aguilar, Gerard, Imperiale, Michael, Funk, Walter, and Abo, Arie
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- 2007
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29. Dissemination of a Web-Based Tool for Supporting Health Insurance Plan Decisions (Show Me Health Plans): Cross-Sectional Observational Study.
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Zhao1, Jingsong, Mir, Nageen, Ackermann, Nicole, Kaphingst, Kimberly A, Politi, Mary C, and Zhao, Jingsong
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HEALTH insurance ,RANDOMIZED controlled trials ,PATIENT Protection & Affordable Care Act ,HEALTH literacy ,PUBLIC health - Abstract
Background: The rate of uninsured people has decreased dramatically since the Affordable Care Act was passed. To make an informed decision, consumers need assistance to understand the advantages and disadvantages of health insurance plans. The Show Me Health Plans Web-based decision support tool was developed to improve the quality of health insurance selection. In response to the promising effectiveness of Show Me Health Plans in a randomized controlled trial (RCT) and the growing need for Web-based health insurance decision support, the study team used expert recommendations for dissemination and implementation, engaged external stakeholders, and made the Show Me Health Plans tool available to the public.Objective: The purpose of this study was to implement the public dissemination of the Show Me Health Plans tool in the state of Missouri and to evaluate its impact compared to the RCT.Methods: This study used a cross-sectional observational design. Dissemination phase users were compared with users in the RCT study across the same outcome measures. Time spent using the Show Me Health Plans tool, knowledge, importance rating of 9 health insurance features, and intended plan choice match with algorithm predictions were examined.Results: During the dissemination phase (November 2016 to January 2017), 10,180 individuals visited the SMHP website, and the 1069 users who stayed on the tool for more than one second were included in our analyses. Dissemination phase users were more likely to live outside St. Louis City or County (P<.001), were less likely to be below the federal poverty level (P<.001), and had a higher income (P=.03). Overall, Show Me Health Plans users from St. Louis City or County spent more time on the Show Me Health Plans tool than those from other Missouri counties (P=.04); this association was not observed in the RCT. Total time spent on the tool was not correlated with knowledge scores, which were associated with lower poverty levels (P=.009). The users from the RCT phase were more likely to select an insurance plan that matched the tool's recommendations (P<.001) compared with the dissemination phase users.Conclusions: The study suggests that a higher income population may be more likely to seek information and online help when making a health insurance plan decision. We found that Show Me Health Plans users in the dissemination phase were more selective in the information they reviewed. This study illustrates one way of disseminating and implementing an empirically tested Web-based decision aid tool. Distributing Web-based tools is feasible and may attract a large number of potential users, educate them on basic health insurance information, and make recommendations based on personal information and preference. However, using Web-based tools may differ according to the demographics of the general public compared to research study participants. [ABSTRACT FROM AUTHOR]- Published
- 2018
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30. Mitogenic Influence of Human R-Spondin 1 on the Intestinal Epithelium.
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Kim, Kyung-Ah, Kakitani, Makoto, Zhao, Jingsong, Oshima, Takeshi, Tang, Tom, Binnerts, Minke, Liu, Yi, Boyle, Bryan, Park, Emily, Emtage, Peter, Funk, Walter D., and Tomizuka, Kazuma
- Subjects
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MITOGENS , *EPITHELIAL cells , *CYTOLOGY , *GENE expression , *GENETIC regulation , *GASTROINTESTINAL agents - Abstract
Several described growth factors influence the proliferation and regeneration of the intestinal epithelium. Using a transgenic mouse model, we identified a human gene, R-spondin1, with potent and specific proliferative effects on intestinal crypt cells. Human R-spondin1 (hRSpo1) is a thrombospondin domain-containing protein expressed in enteroendocrine cells as well as in epithelial cells in various tissues. Upon injection into mice, the protein induced rapid onset of crypt cell proliferation involving β-catenin stabilization, possibly by a process that is distinct from the canonical Wnt-mediated signaling pathway. The protein also displayed efficacy in a model of chemotherapy-induced intestinal mucositis and may have therapeutic application in gastrointestinal diseases. [ABSTRACT FROM AUTHOR]
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- 2005
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31. Erratum to “TACE is required for fetal murine cardiac development and modeling” [Dev. Biol. 261 (2003) 371–380]
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Shi, Wei, Chen, Hui, Sun, Jianping, Buckley, Sue, Zhao, Jingsong, Anderson, Kathryn D., Williams, Roberta G., and Warburton, David
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- 2004
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32. Exosomes carried miR-181c-5p alleviates neuropathic pain in CCI rat models.
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Zhang YU, Ye G, Zhao J, Chen Y, Kong L, Sheng C, and Yuan L
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- Animals, Inflammation metabolism, Rats, Rats, Sprague-Dawley, Exosomes metabolism, MicroRNAs genetics, MicroRNAs metabolism, Neuralgia genetics, Neuralgia metabolism
- Abstract
Mesenchymal stem cells (MSCs) derived exosomes (Exos) are one of the most promising candidate for the treatment of this condition. However, the underlying molecular mechanism remains uncertain. Here we investigated the therapeutic effect of exosomal miR-181c-5p (ExomiR-181c-5p) on a rat model of neuropathic pain induced by sciatic nerve chronic constriction injury (CCI). In this study NP model was established using the CCI method. NP levels were assessed using PWT and PWL. Microarray analysis and RT-PCR were used to determine the relative expression of miR-181c-5p. MSC-derived exosomes were extracted using the total exosome isolation reagent characterized by WB and NTA. MiR-181c-5p was loading into Exos using electroporation. The inflammation response in microglia cells and CCI rats were assessed by ELISA assay respectively. Our study demonstrates that miR-181c-5p expression was obviously decreased in a time-dependent manner in CCI rats. MiR-181c-5p was effectively electroporated and highly detected in MSC-derived Exos. ExomiR-181c-5p internalized by microglia cells and inhibit the secretion of inflammation factors. ExomiR-181c-5p intrathecal administration alleviated neuropathic pain and neuroinflammation response in CCI rats. Taken together, ExomiR-181c-5p alleviated CCI-induced NP by inhibiting neuropathic inflammation. ExomiR-181c-5p may be a valid alternative for the treatment of neuropathic pain and has vast potential for future development.
- Published
- 2022
- Full Text
- View/download PDF
33. A Novel Allosteric Insulin Receptor-Activating Antibody Reduces Hyperglycemia without Hypoglycemia in Diabetic Cynomolgus Monkeys.
- Author
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Bezwada P, Zhao J, Der K, Shimizu B, Cao L, Ahene A, Rubin P, and Johnson K
- Subjects
- Animals, Antibodies pharmacology, Antibodies therapeutic use, Blood Glucose drug effects, Blood Glucose metabolism, Diabetes Mellitus, Type 2 drug therapy, Female, Hyperglycemia drug therapy, Hypoglycemia drug therapy, Hypoglycemic Agents pharmacology, Macaca fascicularis, Male, Receptor, Insulin agonists, Antigens, CD metabolism, Diabetes Mellitus, Type 2 blood, Hyperglycemia blood, Hypoglycemia blood, Hypoglycemic Agents therapeutic use, Receptor, Insulin metabolism
- Abstract
XMetA is a fully human, allosteric monoclonal antibody that binds the insulin receptor with high affinity and mimics the glucoregulatory, but not the mitogenic, actions of insulin. Here we evaluated the efficacy of both single and repeat s.c. administrations of XMetA in reducing hyperglycemia in obese cynomolgus monkeys with naturally developed type 2 diabetes, a model that shares many features of human diabetes. The data show that a single s.c. administration of XMetA at dose levels ranging from 1.5 to 10 mg/kg markedly reduced fasting hyperglycemia, with a peak effect occurring 1 to 2 days after administration, and sustained for up to 1 week. XMetA's effect on hyperglycemia was observed without elevations in serum insulin and was concomitant with reduced serum C-peptide levels, even at the lowest dose. Subchronic effects were evaluated via once weekly s.c. administration of XMetA, 10 mg/kg, for 6 weeks. XMetA treatment resulted in robust weekly decreases in fasting glucose levels averaging approximately 30% throughout the study, along with a significant absolute reduction from the vehicle control baseline of 1.2% in hemoglobin A1c, a marker of long-term glycemic status. XMetA treatment was well tolerated with no injection-site reactions, no body weight gain, and no episodes of clinical hypoglycemia. Thus, XMetA shows acute and subchronic improvements in glycemic control in spontaneously diabetic cynomolgus monkeys with a broad safety margin. This profile supports the development of XMetA as a novel glucose-lowering therapeutic agent for the management of type 2 diabetes., (Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.)
- Published
- 2016
- Full Text
- View/download PDF
34. Targeting C-type lectin-like molecule-1 for antibody-mediated immunotherapy in acute myeloid leukemia.
- Author
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Zhao X, Singh S, Pardoux C, Zhao J, Hsi ED, Abo A, and Korver W
- Subjects
- Animals, Antibodies, Monoclonal biosynthesis, Antibodies, Monoclonal toxicity, CHO Cells, Cell Line, Cricetinae, Cricetulus, HL-60 Cells, Humans, Leukemia, Myeloid, Acute metabolism, Mice, Mice, Inbred BALB C, Mice, SCID, Protein Transport immunology, Receptors, Mitogen, Xenograft Model Antitumor Assays methods, Antibodies, Monoclonal therapeutic use, Immunotherapy methods, Lectins, C-Type immunology, Lectins, C-Type metabolism, Leukemia, Myeloid, Acute immunology, Leukemia, Myeloid, Acute therapy
- Abstract
Background: C-type lectin-like molecule-1 is a transmembrane receptor expressed on myeloid cells, acute myeloid leukemia blasts and leukemic stem cells. To validate the potential of this receptor as a therapeutic target in acute myeloid leukemia, we generated a series of monoclonal antibodies against the extracellular domain of C-type lectin-like molecule-1 and used them to extend the expression profile analysis of acute myeloid leukemia cells and to select cytotoxic monoclonal antibodies against acute myeloid leukemia cells in preclinical models., Design and Methods: C-type lectin-like molecule-1 expression was analyzed in acute myeloid leukemia cell lines, and in myeloid derived cells from patients with acute myeloid leukemia and healthy donors. Anti-C-type lectin-like molecule-1 antibody-mediated in vitro cytotoxic activity against acute myeloid leukemia blasts/cell lines and in vivo anti-cancer activity in a mouse xenograft model were assessed. Internalization of C-type lectin-like molecule-1 monoclonal antibodies upon receptor ligation was also investigated., Results: C-type lectin-like molecule-1 was expressed in 86.5% (45/52) of cases of acute myeloid leukemia, in 54.5% (12/22) of acute myeloid leukemia CD34(+)/CD38(-) stem cells, but not in acute lymphoblastic leukemia blasts (n=5). Selected anti-C-type lectin-like molecule-1 monoclonal antibodies mediated dose-dependent complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity specifically against acute myeloid leukemia-derived cell lines. Exogenous expression of the transmembrane receptor in HEK293 cells rendered the cells susceptible to antibody-mediated killing by monoclonal antibodies to the receptor. Furthermore, these monoclonal antibodies demonstrated strong complement-dependent cytotoxicity against freshly isolated acute myeloid leukemia blasts (15/16 cases; 94%). The monoclonal antibodies were efficiently internalized upon binding to C-type lectin-like molecule-1 in HL-60 cells. Moreover, a lead chimeric C-type lectin-like molecule-1 monoclonal antibody reduced the tumor size in xenograft mice implanted with HL-60 cells. Conclusions Our results demonstrate that targeting C-type lectin-like molecule-1 with specific cytotoxic monoclonal antibodies is an attractive approach which could lead to novel therapies for acute myeloid leukemia.
- Published
- 2010
- Full Text
- View/download PDF
35. rNAPc2 inhibits colorectal cancer in mice through tissue factor.
- Author
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Zhao J, Aguilar G, Palencia S, Newton E, and Abo A
- Subjects
- Animals, Antibodies, Monoclonal therapeutic use, Antibodies, Monoclonal, Humanized, Bevacizumab, Cell Line, Tumor, Colorectal Neoplasms pathology, Disease Progression, Female, Fluorouracil therapeutic use, Humans, Intestinal Neoplasms prevention & control, Lung Neoplasms prevention & control, Lung Neoplasms secondary, Mice, Mice, Inbred BALB C, Mice, Nude, Xenograft Model Antitumor Assays, Colorectal Neoplasms drug therapy, Helminth Proteins pharmacology, Thromboplastin physiology
- Abstract
Purpose: Recombinant nematode anticoagulant protein c2 (rNAPc2) is a specific inhibitor of tissue factor (TF)/factor VIIa complex with novel antithrombotic activity. TF is highly expressed in human colorectal tumors, and levels are positively correlated with disease progression., Experimental Design: To explore the therapeutic potential and mechanism of action of rNAPc2 during tumor growth and metastasis, we tested rNAPc2 in several experimental colorectal cancer models in mice., Results: Administration of rNAPc2 inhibited pulmonary metastasis in mice systemically disseminated with CT26 murine colon carcinoma cells in a dose-dependent fashion. Combining rNAPc2 with the cytotoxic agent 5-fluorouracil or bevacizumab (humanized anti-vascular endothelial growth factor monoclonal antibody) resulted in additive growth inhibition and simultaneous reduction of microvessel density in HCT116 human colorectal tumor xenografts in nude mice. Furthermore, rNAPc2 potentiated CPT-11 in inhibiting hepatic metastasis in nude mice with portal vein injection of HCT116 tumor cells. Long-term administration of rNAPc2 significantly suppressed spontaneous formation of intestinal tumors in Apc(Min/+) mice. Using a RNA interference approach, we showed that TF expression is necessary for rNAPc2-mediated inhibition of HCT116 human colorectal tumor xenograft growth in nude mice, indicating that the antitumor effect of rNAPc2 may be transduced through TF that is expressed on tumor cells., Conclusions: rNAPc2 is a potent anticancer agent when used in combination with chemotherapy or antiangiogenic therapy in mouse models of colorectal cancer, and TF positivity appears to be required for its activity.
- Published
- 2009
- Full Text
- View/download PDF
36. Oral RDP58 allows CPT-11 dose intensification for enhanced tumor response by decreasing gastrointestinal toxicity.
- Author
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Zhao J, Huang L, Belmar N, Buelow R, and Fong T
- Subjects
- Administration, Oral, Animals, Antineoplastic Agents, Phytogenic administration & dosage, Camptothecin toxicity, Cell Line, Tumor, Cytokines biosynthesis, Cytokines metabolism, Digestive System drug effects, Dose-Response Relationship, Drug, Female, Fluorouracil administration & dosage, Intestinal Mucosa metabolism, Irinotecan, Jejunum metabolism, Mice, Mice, Inbred BALB C, Neoplasm Metastasis, Peptides chemistry, Peptides toxicity, Time Factors, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Camptothecin administration & dosage, Camptothecin analogs & derivatives, Histocompatibility Antigens Class I, Peptides administration & dosage
- Abstract
Cancer patients undergoing triple therapy (CPT-11, 5-fluorouracil, and leucovorin) often present with severe delayed diarrhea as a result of chemotherapy-induced gastrointestinal (GI) toxicity and inflammation. RDP58 is a novel, anti-inflammatory, D-amino acid decapeptide that inhibits the production of tumor necrosis factor alpha, IFN-gamma, and interleukin 12, and has been shown to effectively inhibit clinical symptoms and intestinal inflammation in several rodent models of chemically induced colitis, nonhuman primates with spontaneous colitis, and humans with mild to moderate ulcerative colitis. We evaluated RDP58 as a potential protective agent in chemotherapy-induced GI inflammation. Oral administration of RDP58 significantly decreased the incidence of diarrhea and improved the survival rates of mice treated with toxic doses of CPT-11 or 5-fluorouracil. Histological analysis showed that RDP58 significantly reduced the destruction of the intestinal mucosa by inhibiting local overproduction of tumor necrosis factor alpha, IFN-gamma, and interleukin 12 in vivo. Furthermore, RDP58 administration allowed the maximum tolerated dose of CPT-11 to be doubled in tumor-bearing mice resulting in significantly enhanced primary tumor responses and prolongation of time to relapse without a concomitant increase in GI toxicity. Our results suggest that RDP58 may have clinical utility in cancer therapy by preventing treatment-associated GI toxicity and potentially increasing the effectiveness of chemotherapy.
- Published
- 2004
- Full Text
- View/download PDF
37. Overexpression of Smurf1 negatively regulates mouse embryonic lung branching morphogenesis by specifically reducing Smad1 and Smad5 proteins.
- Author
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Shi W, Chen H, Sun J, Chen C, Zhao J, Wang YL, Anderson KD, and Warburton D
- Subjects
- Animals, Bone Morphogenetic Protein 4, Bone Morphogenetic Proteins metabolism, Cell Differentiation physiology, Cell Division physiology, Cell Line, Tumor, Female, Gene Expression Regulation, Developmental, Lung cytology, Lung Neoplasms, Mice, Phosphoproteins genetics, Pregnancy, Smad Proteins, Smad1 Protein, Smad5 Protein, DNA-Binding Proteins genetics, Lung embryology, Lung physiology, Trans-Activators genetics, Ubiquitin-Protein Ligases genetics
- Abstract
Early embryonic lung branching morphogenesis is regulated by many growth factor-mediated pathways. Bone morphogenetic protein 4 (BMP4) is one of the morphogens that stimulate epithelial branching in mouse embryonic lung explant culture. To further understand the molecular mechanisms of BMP4-regulated lung development, we studied the biological role of Smad-ubiquitin regulatory factor 1 (Smurf1), an ubiquitin ligase specific for BMP receptor-regulated Smads, during mouse lung development. The temporo-spatial expression pattern of Smurf1 in mouse embryonic lung was first determined by quantitative real-time PCR and immunohistochemistry. Overexpression of Smurf1 in airway epithelial cells by intratracheal introduction of recombinant adenoviral vector dramatically inhibited embryonic day (E) 11.5 lung explant growth in vitro. This inhibition of lung epithelial branching was restored by coexpression of Smad1 or by addition of soluble BMP4 ligand into the culture medium. Studies at the cellular level show that overexpression of Smurf1 reduced epithelial cell proliferation and differentiation, as documented by reduced PCNA-positive cell index and by reduced mRNA levels for surfactant protein C and Clara cell protein 10 expression. Further studies found that overexpression of Smurf1 reduced BMP-specific Smad1 and Smad5, but not Smad8, protein levels. Thus overexpression of Smurf1 specifically promotes Smad1 and Smad5 ubiquitination and degradation in embryonic lung epithelium, thereby modulating the effects of BMP4 on embryonic lung growth.
- Published
- 2004
- Full Text
- View/download PDF
38. Smad3 deficiency attenuates bleomycin-induced pulmonary fibrosis in mice.
- Author
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Zhao J, Shi W, Wang YL, Chen H, Bringas P Jr, Datto MB, Frederick JP, Wang XF, and Warburton D
- Subjects
- Animals, Collagen metabolism, DNA-Binding Proteins genetics, Fibronectins metabolism, Lung metabolism, Lung pathology, Mice, Mice, Knockout genetics, Pulmonary Fibrosis metabolism, Smad3 Protein, Trans-Activators genetics, Bleomycin, DNA-Binding Proteins deficiency, Pulmonary Fibrosis chemically induced, Pulmonary Fibrosis pathology, Trans-Activators deficiency
- Abstract
Transforming growth factor-beta (TGF-beta) signaling plays an important regulatory role during lung fibrogenesis. Smad3 was identified in the pathway for transducing TGF-beta signals from the cell membrane to the nucleus. Using mice without Smad3 gene expression, we investigated whether Smad3 could regulate bleomycin-induced pulmonary fibrosis in vivo. Mice deficient in Smad3 demonstrated suppressed type I procollagen mRNA expression and reduced hydroxyproline content in the lungs compared with wild-type mice treated with bleomycin. Furthermore, loss of Smad3 greatly attenuated morphological fibrotic responses to bleomycin in the mouse lungs, suggesting that Smad3 is implicated in the pathogenesis of pulmonary fibrosis. These results show that Smad3 contributes to bleomycin-induced lung injury and that Smad3 may serve as a novel target for potential therapeutic treatment of lung fibrosis.
- Published
- 2002
- Full Text
- View/download PDF
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