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2. Divalent siRNAs are bioavailable in the lung and efficiently block SARS-CoV-2 infection

Author

Hariharan, Vignesh N., primary, Shin, Minwook, additional, Chang, Ching-Wen, additional, O’Reilly, Daniel, additional, Biscans, Annabelle, additional, Yamada, Ken, additional, Guo, Zhiru, additional, Somasundaran, Mohan, additional, Tang, Qi, additional, Monopoli, Kathryn, additional, Krishnamurthy, Pranathi Meda, additional, Devi, Gitali, additional, McHugh, Nicholas, additional, Cooper, David A., additional, Echeverria, Dimas, additional, Cruz, John, additional, Chan, Io Long, additional, Liu, Ping, additional, Lim, Sun-Young, additional, McConnell, Jill, additional, Singh, Satya Prakash, additional, Hildebrand, Samuel, additional, Sousa, Jacquelyn, additional, Davis, Sarah M., additional, Kennedy, Zachary, additional, Ferguson, Chantal, additional, Godinho, Bruno M. D. C., additional, Thillier, Yann, additional, Caiazzi, Jillian, additional, Ly, Socheata, additional, Muhuri, Manish, additional, Kelly, Karen, additional, Humphries, Fiachra, additional, Cousineau, Alyssa, additional, Parsi, Krishna Mohan, additional, Li, Qi, additional, Wang, Yang, additional, Maehr, René, additional, Gao, Guangping, additional, Korkin, Dmitry, additional, McDougall, William M., additional, Finberg, Robert W., additional, Fitzgerald, Katherine A., additional, Wang, Jennifer P., additional, Watts, Jonathan K., additional, and Khvorova, Anastasia, additional

Published
2023
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3. An Early Islet Transcriptional Signature Is Associated With Local Inflammation in Autoimmune Diabetes

Author

Derr, Alan G., primary, Arowosegbe, Adediwura, additional, Satish, Basanthi, additional, Redick, Sambra D., additional, Qaisar, Natasha, additional, Guo, Zhiru, additional, Vanderleeden, Emma, additional, Trombly, Melanie I., additional, Baer, Christina E., additional, Harlan, David M., additional, Greiner, Dale L., additional, Garber, Manuel, additional, and Wang, Jennifer P., additional

Published
2022
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6. An Early Islet Transcriptional Signature is Associated with Local Inflammation in Autoimmune Diabetes.

Author

Derr, Alan G., Arowosegbe, Adediwura, Satish, Basanthi, Redick, Sambra D., Qaisar, Natasha, Guo, Zhiru, Vanderleeden, Emma, Trombly, Melanie I., Baer, Christina E., Harlan, David M., Greiner, Dale L., Garber, Manuel, and Wang, Jennifer P.

Subjects
ISLANDS, TYPE 1 diabetes, MACROPHAGES, INSULINOMA, AUTOIMMUNITY, ISLANDS of Langerhans, AUTOIMMUNE diseases
Abstract

Identifying the early islet cellular processes of autoimmune type 1 diabetes (T1D) in humans is challenging given the absence of symptoms during this period and the inaccessibility of the pancreas for sampling. Here, we study temporal events in pancreatic islets in LEW.1WR1 rats, in which autoimmune diabetes can be induced with virus infection, by performing transcriptional analysis of islets harvested during the pre-diabetic period. Single-cell RNA-Seq and differential expression analyses of islets from pre-diabetic rats reveal subsets of β and α cells under stress as evidenced by heightened expression, over time, of a transcriptional signature characterized by interferon-stimulated genes, chemokines including Cxcl10, major histocompatibility class I, and genes for the ubiquitin-proteasome system. Mononuclear phagocytes show increased expression of inflammatory markers. RNA-in situ hybridization of rat pancreatic tissue defines the spatial distribution of Cxcl10+ β and α cells and their association with CD8+ T cell infiltration, a hallmark of insulitis and islet destruction. Our studies define early islet transcriptional events during immune cell recruitment to islets and reveal spatial associations between stressed β and α cells and immune cells. Insights into such early processes can assist in the development of therapeutic and prevention strategies for T1D. [ABSTRACT FROM AUTHOR]

Published
2023
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11. Arachidonate 15-lipoxygenase is required for chronic myeloid leukemia stem cell survival

Author

Chen, Yaoyu, Peng, Cong, Abraham, Sheela A., Shan, Yi, Guo, Zhiru, Desouza, Ngoc, Cheloni, Giulia, Li, Dongguang, Holyoake, Tessa L., and Li, Shaoguang

Subjects
Stem cells -- Research -- Physiological aspects, Chronic myeloid leukemia -- Development and progression -- Research -- Risk factors -- Patient outcomes -- Complications and side effects, Health care industry
Abstract

Cancer stem cells (CSCs) are responsible for the initiation and maintenance of some types of cancer, suggesting that inhibition of these cells may limit disease progression and relapse. Unfortunately, few CSC-specific genes have been identified. Here, we determined that the gene encoding arachidonate 15-lipoxygenase (Alox15/15-LO) is essential for the survival of leukemia stem cells (LSCs) in a murine model of BCR-ABL-induced chronic myeloid leukemia (CML). In the absence of Alox15, BCRABL was unable to induce CML in mice. Furthermore, Alox15 deletion impaired LSC function by affecting cell division and apoptosis, leading to an eventual depletion of LSCs. Moreover, chemical inhibition of 15-LO function impaired LSC function and attenuated CML in mice. The defective CML phenotype in Alox15-deficient animals was rescued by depleting the gene encoding P-selectin, which is upregulated in Alox15-deficient animals. Both deletion and overexpression of P-selectin affected the survival of LSCs. In human CML cell lines and [CD34.sup.+] cells, knockdown of Alox15 or inhibition of 15-LO dramatically reduced survival. Loss of Alox15 altered expression of PTEN, PI3K/AKT, and the transcription factor ICSBP, which are known mediators of cancer pathogenesis. These results suggest that ALOX15 has potential as a therapeutic target for eradicating LSCs in CML., Introduction Cancer stem cells (CSCs) in a variety of hematologic malignancies and some solid tumors are required for cancer initiation and are responsible for disease relapse (1-7). Accumulating evidence suggests [...]

Published
2014
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13. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues

Author

Ziegler, Carly G.K., primary, Allon, Samuel J., additional, Nyquist, Sarah K., additional, Mbano, Ian M., additional, Miao, Vincent N., additional, Tzouanas, Constantine N., additional, Cao, Yuming, additional, Yousif, Ashraf S., additional, Bals, Julia, additional, Hauser, Blake M., additional, Feldman, Jared, additional, Muus, Christoph, additional, Wadsworth, Marc H., additional, Kazer, Samuel W., additional, Hughes, Travis K., additional, Doran, Benjamin, additional, Gatter, G. James, additional, Vukovic, Marko, additional, Taliaferro, Faith, additional, Mead, Benjamin E., additional, Guo, Zhiru, additional, Wang, Jennifer P., additional, Gras, Delphine, additional, Plaisant, Magali, additional, Ansari, Meshal, additional, Angelidis, Ilias, additional, Adler, Heiko, additional, Sucre, Jennifer M.S., additional, Taylor, Chase J., additional, Lin, Brian, additional, Waghray, Avinash, additional, Mitsialis, Vanessa, additional, Dwyer, Daniel F., additional, Buchheit, Kathleen M., additional, Boyce, Joshua A., additional, Barrett, Nora A., additional, Laidlaw, Tanya M., additional, Carroll, Shaina L., additional, Colonna, Lucrezia, additional, Tkachev, Victor, additional, Peterson, Christopher W., additional, Yu, Alison, additional, Zheng, Hengqi Betty, additional, Gideon, Hannah P., additional, Winchell, Caylin G., additional, Lin, Philana Ling, additional, Bingle, Colin D., additional, Snapper, Scott B., additional, Kropski, Jonathan A., additional, Theis, Fabian J., additional, Schiller, Herbert B., additional, Zaragosi, Laure-Emmanuelle, additional, Barbry, Pascal, additional, Leslie, Alasdair, additional, Kiem, Hans-Peter, additional, Flynn, JoAnne L., additional, Fortune, Sarah M., additional, Berger, Bonnie, additional, Finberg, Robert W., additional, Kean, Leslie S., additional, Garber, Manuel, additional, Schmidt, Aaron G., additional, Lingwood, Daniel, additional, Shalek, Alex K., additional, Ordovas-Montanes, Jose, additional, Banovich, Nicholas, additional, Brazma, Alvis, additional, Desai, Tushar, additional, Duong, Thu Elizabeth, additional, Eickelberg, Oliver, additional, Falk, Christine, additional, Farzan, Michael, additional, Glass, Ian, additional, Haniffa, Muzlifah, additional, Horvath, Peter, additional, Hung, Deborah, additional, Kaminski, Naftali, additional, Krasnow, Mark, additional, Kuhnemund, Malte, additional, Lafyatis, Robert, additional, Lee, Haeock, additional, Leroy, Sylvie, additional, Linnarson, Sten, additional, Lundeberg, Joakim, additional, Meyer, Kerstin, additional, Misharin, Alexander, additional, Nawijn, Martijn, additional, Nikolic, Marko Z., additional, Pe’er, Dana, additional, Powell, Joseph, additional, Quake, Stephen, additional, Rajagopal, Jay, additional, Tata, Purushothama Rao, additional, Rawlins, Emma L., additional, Regev, Aviv, additional, Reyfman, Paul A., additional, Rojas, Mauricio, additional, Rosen, Orit, additional, Saeb-Parsy, Kourosh, additional, Samakovlis, Christos, additional, Schiller, Herbert, additional, Schultze, Joachim L., additional, Seibold, Max A., additional, Shepherd, Douglas, additional, Spence, Jason, additional, Spira, Avrum, additional, Sun, Xin, additional, Teichmann, Sarah, additional, Theis, Fabian, additional, Tsankov, Alexander, additional, van den Berge, Maarten, additional, von Papen, Michael, additional, Whitsett, Jeffrey, additional, Xavier, Ramnik, additional, Xu, Yan, additional, and Zhang, Kun, additional

Published
2020
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15. Identification of Zika Virus and Dengue Virus Dependency Factors using Functional Genomics

Author

Savidis, George, primary, McDougall, William M., additional, Meraner, Paul, additional, Perreira, Jill M., additional, Portmann, Jocelyn M., additional, Trincucci, Gaia, additional, John, Sinu P., additional, Aker, Aaron M., additional, Renzette, Nicholas, additional, Robbins, Douglas R., additional, Guo, Zhiru, additional, Green, Sharone, additional, Kowalik, Timothy F., additional, and Brass, Abraham L., additional

Published
2016
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16. The IFITMs Inhibit Zika Virus Replication

Author

Savidis, George, primary, Perreira, Jill M., additional, Portmann, Jocelyn M., additional, Meraner, Paul, additional, Guo, Zhiru, additional, Green, Sharone, additional, and Brass, Abraham L., additional

Published
2016
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22. Inhibition of foot-and-mouth disease virus replication in vitro and in vivo by small interfering RNA.

Author

Wang Pengyan, Ren Yan, Guo Zhiru, and Chen Chuangfu

Subjects
FOOT & mouth disease, SMALL interfering RNA, GENOMES, PLASMIDS, SEROTYPES, ANIMAL models in research
Abstract

By using bioinformatics computer programs, all foot-and-mouth disease virus (FMDV) genome sequences in public-domain databases were analyzed. Based on the results of homology analysis, 2 specific small interfering RNA (siRNA) targeting homogenous 3D and 2B1 regions of 7 serotypes of FMDV were prepared and 2 siRNA-expression vectors, pSi-FMD2 and pSi-FMD3, were constructed. The siRNA-expressing vectors were used to test the ability of siRNAs to inhibit virus replication in baby hamster kidney (BHK-21) cells and suckling mice, a commonly used small animal model. The results demonstrated that transfection of BHK-21 cells with siRNA-expressing plasmids significantly weakened the cytopathic effect (CPE). Moreover, BHK-21 cells transiently transfected with short hairpin RNA (shRNA)-expressing plasmids were specifically resistant to the infection of the FMDV serotypes A, O, and Asia I and this the antiviral effects persisted for almost 48 hours. We measured the viral titers, the 50% tissue culture infective dose (TCID50) in cells transfected with anti-FMDV siRNAs was found to be lower than that of the control cells. Furthermore, subcutaneous injection of siRNA-expressing plasmids in the neck of the suckling mice made them less susceptible to infection with O, and Asia I serotypes of FMDV. [ABSTRACT FROM AUTHOR]

Published
2008
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24. Genetic and Pharmacologic Targeting Of Alox5 Attenuates JAK2V617FInduced PV In Mice

Author

Chen, Yaoyu, Shan, Yi, Guo, Zhiru, Liang, Aibin, and Li, Shaoguang

Abstract

The myeloproliferative neoplasms (MPNs) are hematologic malignancies with a chronic clinical course and a risk of developing thrombosis and acute leukemia. JAK2 is a member of the Janus family of non-receptor tyrosine kinases, and the somatic activating point mutation of JAK2(JAK2V617F) has been found in Philadelphia chromosome-negative MPNs in approximately 95% of polycythemia (PV), 60% of essential thrombocytosis (ET), and 50% of JAK2 V617F-positive MPD (PMF) patients. Although several JAK2 inhibitors are in the early stage of clinical trials and have been shown to help to improve symptoms and quality of life in patients, their long-term effectiveness in patients remains to be determined. New therapeutic strategies need to be developed for treating PV more effectively. Because hematopoietic stem cells (HSCs) harbor JAK2V617Fin PV patients, PV should be compared to Philadelphia chromosome-positive chronic myeloid leukemia (CML) that is also derived from HSCs and has a myeloproliferative phenotype similar to PV in mice. Therefore, we reasoned that a gene essential for CML development might also play a critical role in PV development. We have shown that the survival and self-renewal of CML-initiating cells require the arachidonate 5-lipoxygenase gene (Alox5) and that Alox5is essential for CML development. Therefore, in this study we investigated the role of Alox5in pathogenesis of PV in mice. We showed that JAK2V617Fupregulates Alox5 expression both in vitro(Ba/F3 cells) and in vivo(the spleen cells in PV mice). To examine whether Alox5 is required for induction of PV by JAK2V617F, we transduced bone marrow (BM) cells from wild type (WT) or Alox5homozygous knockout (Alox5-/-) mice with JAK2V617F-GFP, followed by transplantation into lethally-irradiated recipient mice. We found that the average percentage of JAK2V617F-expressing white blood cell counts (GFP+WBCs) in recipients of JAK2V617F-transduced Alox5-/-donor BM cells was significantly lower than that in recipients of JAK2V617F-transduced WT donor BM cells (P< 0.001). Total numbers of WBCs, red blood cells (RBCs), hemoglobin (HGB) and hematocrit (HCT) were also significantly lower in the absence of Alox5. With time (at 9 months after induction of PV), the effect of Alox5deficiency on PV development became more significant. Because JAK2V617F-transformed HSCs is shown to be a PV-initiating cell population, we further tested whether loss of Alox5affects this cell population in PV mice. We found that the percentage and total number of HSCs (Lin-Sca-1+c-Kit+) in mice receiving JAK2V617F-transduced Alox5-/-BM cells was significantly lower than that in mice receiving JAK2V617F-transduced WT BM cells. These findings suggest that Alox5 could be an effective target gene for PV. We tested this idea by treating PV mice with an Alox5 inhibitor zileuton (300 mg/kg, once a day) or a placebo. Western blot analysis of protein lysates from the spleens of PV mice showed that 5-lipoxygines (5-LO, a protein product of the Alox5gene) is upregulated by JAK2V617F, and inhibition of Alox5 function by zileuton restored the 5-LO level back to the control level. In addition, the number of WBCs in placebo-treated mice rose significantly with time, whereas the number of WBCs in zileuton-treated mice did not. The inhibition of PV development by zileuton correlated with much smaller infiltrated spleen in zileuton-treated PV mice than in placebo-treated PV mice. Furthermore, we compared the levels of JAK2V617F-expressing cells (GFP+) in PV mice. FACS analysis showed that the percentage of Gr-1+or Mac+PV cells in peripheral blood was significantly lower in zileuton-treated PV mice than in placebo-treated PV mice. Consistent with the inhibition of PV cells by zileuton in mice, survival of zileuton-treated PV mice was significantly improved compared to placebo-treated PV mice (Fig. 3I). At 5 months after induction of PV, about 40% placebo-treated PV mice died, but all zileuton-treated mice survived. To understand the underlying mechanisms, we treated JAK2V617F-expressing BaF/3 cells with zileuton, and found that zileuton inhibited activation of AKT and β-catenin by JAK2V617F, and did not affect activation of PI3K, MAPK and JAK2. Together, these results demonstrate that Alox5 represents a critical pathway in JAK2V617F-induced PV and that targeting of Alox5 provides a new strategy for treating PV.

Published
2013
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