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2. Novel PET and Near Infrared Imaging Probes for the Specific Detection of Bacterial Infections Associated With Cardiac Devices

Author

Takemiya, Kiyoko, Ning, Xinghai, Seo, Wonewoo, Wang, Xiaojian, Mohammad, Rafi, Joseph, Giji, Titterington, Jane S, Kraft, Colleen S, Nye, Jonathan A, Murthy, Niren, Goodman, Mark M, and Taylor, W Robert

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Infectious Diseases, Biomedical Imaging, Assistive Technology, Bioengineering, Infection, Animals, Disease Models, Animal, Early Diagnosis, Fluorescent Dyes, Fluorine Radioisotopes, Injections, Intravenous, Male, Oligosaccharides, Optical Imaging, Positron-Emission Tomography, Predictive Value of Tests, Prosthesis-Related Infections, Radiopharmaceuticals, Rats, Sprague-Dawley, Reproducibility of Results, Spectroscopy, Near-Infrared, Staphylococcal Infections, Staphylococcus aureus, Time Factors, bacterial imaging, medical device infections, optical imaging, PET, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

ObjectivesThe aim of this study was to develop imaging agents to detect early stage infections in implantable cardiac devices.BackgroundBacteria ingest maltodextrins through the specific maltodextrin transporter. We developed probes conjugated with either a fluorescent dye (maltohexaose fluorescent dye probe [MDP]) or a F-18 (F18 fluoromaltohexaose) and determined their usefulness in a model of infections associated with implanted cardiac devices.MethodsStainless steel mock-ups of medical devices were implanted subcutaneously in rats. On post-operative day 4, animals were injected with either Staphylococcus aureus around the mock-ups to induce a relatively mild infection or oil of turpentine to induce noninfectious inflammation. Animals with a sterile implant were used as control subjects. On post-operative day 6, either the MDP or F18 fluoromaltohexaose was injected intravenously, and the animals were scanned with the appropriate imaging device. Additional positron emission tomography imaging studies were performed with F18-fluorodeoxyglucose as a comparison of the specificity of our probes (n = 5 to 9 per group).ResultsThe accumulation of the MDP in the infected rats was significantly increased at 1 h after injection when compared with the control and noninfectious inflammation groups (intensity ratio 1.54 ± 0.07 vs. 1.26 ± 0.04 and 1.20 ± 0.05, respectively; p < 0.05) and persisted for more than 24 h. In positron emission tomography imaging, both F18 fluoromaltohexaose and F18 fluorodeoxyglucose significantly accumulated in the infected area 30 min after the injection (maximum standard uptake value ratio 4.43 ± 0.30 and 4.87 ± 0.28, respectively). In control rats, there was no accumulation of imaging probes near the device. In the noninfectious inflammation rats, no significant accumulation was observed with F18 fluoromaltohexaose, but F18 fluorodeoxyglucose accumulated in the mock-up area (maximum standard uptake value 2.53 ± 0.39 vs. 4.74 ± 0.46, respectively; p < 0.05).ConclusionsOur results indicate that maltohexaose-based imaging probes are potentially useful for the specific and sensitive diagnosis of infections associated with implantable cardiac devices.

Published
2019

6. Accelerated atherosclerosis in beta-thalassemia

Author

Hurtado, Julian, primary, Sellak, Hassan, additional, Joseph, Giji, additional, Lewis, Caitlin V., additional, Naudin, Crystal R., additional, Garcia, Sergio, additional, Wodicka, James Robert, additional, Archer, David R., additional, and Taylor, W. Robert, additional

Published
2023
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9. Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis

Author

Lewis, Caitlin V., primary, Sellak, Hassan, additional, Sawan, Mariem A., additional, Joseph, Giji, additional, Darby, Trevor M., additional, VanInsberghe, David, additional, Naudin, Crystal R., additional, Archer, David R., additional, Jones, Rheinallt M., additional, and Taylor, W. Robert, additional

Published
2023
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13. Endothelial Poldip2 regulates sepsis-induced lung injury via Rho pathway activation

Author

Dolmatova, Elena V, primary, Forrester, Steven J, additional, Wang, Keke, additional, Ou, Ziwei, additional, Williams, Holly C, additional, Joseph, Giji, additional, Kumar, Sandeep, additional, Valdivia, Alejandra, additional, Kowalczyk, Andrew P, additional, Qu, Hongyan, additional, Jo, Hanjoong, additional, Lassègue, Bernard, additional, Hernandes, Marina S, additional, and Griendling, Kathy K, additional

Published
2021
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15. Endothelial Poldip2 regulates sepsis-induced lung injury via Rho pathway activation.

Author

Dolmatova, Elena V, Forrester, Steven J, Wang, Keke, Ou, Ziwei, Williams, Holly C, Joseph, Giji, Kumar, Sandeep, Valdivia, Alejandra, Kowalczyk, Andrew P, Qu, Hongyan, Jo, Hanjoong, Lassègue, Bernard, Hernandes, Marina S, and Griendling, Kathy K

Subjects
LUNG injuries, KNOCKOUT mice, ENDOTHELIUM diseases, MACROPHAGE inflammatory proteins, ENDOTHELIAL cells, GENE expression
Abstract

Aims Sepsis-induced lung injury is associated with significant morbidity and mortality. Previously, we showed that heterozygous deletion of polymerase δ-interacting protein 2 (Poldip2) was protective against sepsis-induced lung injury. Since endothelial barrier disruption is thought to be the main mechanism of sepsis-induced lung injury, we sought to determine if the observed protection was specifically due to the effect of reduced endothelial Poldip2. Methods and results Endothelial-specific Poldip2 knock-out mice (EC−/−) and their wild-type littermates (EC+/+) were injected with saline or lipopolysaccharide (18 mg/kg) to model sepsis-induced lung injury. At 18 h post-injection mice, were euthanized and bronchoalveolar lavage (BAL) fluid and lung tissue were collected to assess leucocyte infiltration. Poldip2 EC−/− mice showed reduced lung leucocyte infiltration in BAL (0.21 ± 0.9×106 vs. 1.29 ± 1.8×106 cells/mL) and lung tissue (12.7 ± 1.8 vs. 23 ± 3.7% neutrophils of total number of cells) compared to Poldip2 EC+/+ mice. qPCR analysis of the lung tissue revealed a significantly dampened induction of inflammatory gene expression (TNFα 2.23 ± 0.39 vs. 4.15 ± 0.5-fold, IκBα 4.32 ± 1.53 vs. 8.97 ± 1.59-fold), neutrophil chemoattractant gene expression (CXCL1 68.8 ± 29.6 vs. 147 ± 25.7-fold, CXCL2 65 ± 25.6 vs. 215 ± 27.3-fold) and a marker of endothelial activation (VCAM1 1.25 ± 0.25 vs. 3.8 ± 0.38-fold) in Poldip2 EC−/− compared to Poldip2 EC+/+ lungs. An in vitro model using human pulmonary microvascular endothelial cells was used to assess the effect of Poldip2 knock-down on endothelial activation and permeability. TNFα-induced endothelial permeability and VE-cadherin disruption were significantly reduced with siRNA-mediated knock-down of Poldip2 (5 ± 0.5 vs. 17.5 ± 3-fold for permeability, 1.5 ± 0.4 vs. 10.9 ± 1.3-fold for proportion of disrupted VE-cadherin). Poldip2 knock-down altered expression of Rho-GTPase-related genes, which correlated with reduced RhoA activation by TNFα (0.94 ± 0.05 vs. 1.29 ± 0.01 of relative RhoA activity) accompanied by redistribution of active-RhoA staining to the centre of the cell. Conclusion Poldip2 is a potent regulator of endothelial dysfunction during sepsis-induced lung injury, and its endothelium-specific inhibition may provide clinical benefit. [ABSTRACT FROM AUTHOR]

Published
2022
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17. Reactive oxygen species-selective regulation of aortic inflammatory gene expression in Type 2 diabetes

Author

San Martin, Alejandra, Du, Pingfeng, Dikalova, Anna, Lassegue, Bernard, Aleman, Maria, Gongora, Maria Carolina, Brown, Kathryn, Joseph, Giji, Harrison, David G., Taylor, W. Robert, Jo, Hanjoong, and Griendling, Kathy K.

Subjects
Type 2 diabetes -- Research, NADP (Coenzyme) -- Research, Cardiovascular diseases -- Risk factors, Cardiovascular research, Biological sciences
Abstract

Vascular diseases are a major complication of diabetes mellitus (DM), although their etiology is poorly understood. NADPH oxidase-derived reactive oxygen species (ROS) production and inflammation are potential mediators of DM-associated vascular diseases. Using db/db mice as a Type 2 diabetes model, we examined the relationship between NADPH oxidase-derived ROS and vascular inflammation. When compared with control m+/+ mice, aortas from 4- and 12-wk-old db/db mice had higher NADPH oxidase activity and increased superoxide levels, leading to NADPH oxidase-dependent impaired vasodilation at 12 wk. Diabetes progression from 4 to 12 wk led to increased Nox1, Nox4, and [p22.sup.phox] subunit mRNAs and induced the expression of a group of matrix remodeling-related cytokines: connective tissue growth factor (CTGF), bone morphogenetic protein 4 (BMP-4), and osteopontin (OPN). After 8 wk of treatment with the superoxide scavenger Tempol, 12-wk-old db/db mice had lower superoxide production, reduced plasma glucose and lipids, and lower BMP-4 and OPN protein expression when compared with nontreated mice. No changes were observed with Tempol in CTGF or m+/+ mice. The ability of Tempol to reverse ROS production as well as OPN and BMP-4, but not CTGF, induction suggests that DM-induced vascular inflammation involves both ROS-sensitive and -insensitive pathways. vascular inflammation; NADPH oxidases; cytokines; superoxide; metabolic syndrome doi:10.1152/ajpheart.00943.2006

Published
2007

31. Poldip2 promotes postischemic neovascularization of the mouse hindlimb

Author

Amanso, Angélica M., Lassègue, Bernard, Joseph, Giji, Landázuri, Natalia, Long, James S., Weiss, Daiana, Taylor, W. Robert, and Griendling, Kathy K.

Subjects
Heterozygote, Time Factors, Collateral Circulation, Neovascularization, Physiologic, Apoptosis, Transfection, Article, Mitochondrial Proteins, Mice, Ischemia, Human Umbilical Vein Endothelial Cells, Animals, Humans, Muscle, Skeletal, Cells, Cultured, Cell Proliferation, Mice, Knockout, Macrophages, Nuclear Proteins, Hydrogen Peroxide, Recovery of Function, Hindlimb, Disease Models, Animal, Matrix Metalloproteinase 9, Regional Blood Flow, Matrix Metalloproteinase 2, RNA Interference
Abstract

Collateral vessel formation can functionally compensate for obstructive vascular lesions in patients with atherosclerosis. Neovascularization processes are triggered by fluid shear stress, hypoxia, growth factors, chemokines, proteases, and inflammation, as well as reactive oxygen species, in response to ischemia. Polymerase δ-interacting protein 2 (Poldip2) is a multifunctional protein that regulates focal adhesion turnover and vascular smooth muscle cell migration and modifies extracellular matrix composition. We, therefore, tested the hypothesis that loss of Poldip2 impairs collateral formation.The mouse hindlimb ischemia model has been used to understand mechanisms involved in postnatal blood vessel formation. Poldip2(+/-) mice were subjected to femoral artery excision, and functional and morphological analysis of blood vessel formation was performed after injury. Heterozygous deletion of Poldip2 decreased the blood flow recovery and spontaneous running activity at 21 days after injury. H2O2 production, as well as the activity of matrix metalloproteinases-2 and -9, was reduced in these animals compared with Poldip2(+/+) mice. Infiltration of macrophages in the peri-injury muscle was also decreased; however, macrophage phenotype was similar between genotypes. In addition, the formation of capillaries and arterioles was impaired, as was angiogenesis, in agreement with a decrease in proliferation observed in endothelial cells treated with small interfering RNA against Poldip2. Finally, regression of newly formed vessels and apoptosis was more pronounced in Poldip2(+/-) mice.Together, these results suggest that Poldip2 promotes ischemia-induced collateral vessel formation via multiple mechanisms that likely involve reactive oxygen species-dependent activation of matrix metalloproteinase activity, as well as enhanced vascular cell growth and survival.

Published
2014

40. Cellular Encapsulation Enhances Cardiac Repair

Author

Levit, Rebecca D., primary, Landázuri, Natalia, additional, Phelps, Edward A., additional, Brown, Milton E., additional, García, Andrés J., additional, Davis, Michael E., additional, Joseph, Giji, additional, Long, Robert, additional, Safley, Susan A., additional, Suever, Jonathan D., additional, Lyle, Alicia N., additional, Weber, Collin J., additional, and Taylor, W. Robert, additional

Published
2013
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41. Polymerase Delta Interacting Protein 2 Sustains Vascular Structure and Function

Author

Sutliff, Roy L., primary, Hilenski, Lula L., additional, Amanso, Angélica M., additional, Parastatidis, Ioannis, additional, Dikalova, Anna E., additional, Hansen, Laura, additional, Datla, Srinivasa Raju, additional, Long, James S., additional, El-Ali, Alexander M., additional, Joseph, Giji, additional, Gleason, Rudolph L., additional, Taylor, W. Robert, additional, Hart, C. Michael, additional, Griendling, Kathy K., additional, and Lassègue, Bernard, additional

Published
2013
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45. Alginate microencapsulation of human mesenchymal stem cells as a strategy to enhance paracrine-mediated vascular recovery after hindlimb ischaemia

Author

Landázuri, Natalia, primary, Levit, Rebecca D., additional, Joseph, Giji, additional, Ortega-Legaspi, Juan Manuel, additional, Flores, Cristina A., additional, Weiss, Daiana, additional, Sambanis, Athanassios, additional, Weber, Collin J., additional, Safley, Susan A., additional, and Taylor, W. Robert, additional

Published
2012
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