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2. Small Molecule Inhibitors of Nuclear Export and the Amelioration of Lupus by Modulation of Plasma Cell Generation and Survival

Author

Rangel‐Moreno, Javier, primary, Garcia‐Hernandez, Maria de la Luz, additional, Owen, Teresa, additional, Barnard, Jennifer, additional, Becerril‐Villanueva, Enrique, additional, Kashyap, Trinayan, additional, Argueta, Christian, additional, Gamboa‐Dominguez, Armando, additional, Tamir, Sharon, additional, Landesman, Yosef, additional, Goldman, Bruce I., additional, Ritchlin, Christopher T., additional, and Anolik, Jennifer H., additional

Published
2022
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6. Reviving the Hospital Autopsy

Author

Goldman, Bruce I.

Subjects
Health
Abstract

To the Editor.--The observations of Stephen Geller, MD, on the current state of the hospital autopsy in the United States (1) are very familiar to me, as my colleagues and [...]

Published
2016
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13. Inhibition of G protein βγ subunit signaling abrogates nephritis in lupus prone mice

Author

Rangel-Moreno, Javier, To, Jesi Y., Owen, Teresa, Goldman, Bruce I., Smrcka, Alan V., and Anolik, Jennifer H.

Subjects
Mice, Nephritis, Mice, Inbred NZB, Xanthenes, GTP-Binding Protein gamma Subunits, GTP-Binding Protein beta Subunits, Animals, Lupus Erythematosus, Systemic, Female, Article, Signal Transduction
Abstract

Despite considerable advances in the understanding of systemic lupus erythematosus (SLE), there is still an urgent need for new and more targeted treatment approaches. We previously demonstrated that small-molecule blockade of G protein βγ subunit (Gβγ) signaling inhibits acute inflammation through inhibition of chemokine receptor signal transduction. We undertook this study to determine whether inhibition of Gβγ signaling ameliorates disease in a mouse model of SLE.Lupus-prone (NZB × NZW)F1 female mice were prophylactically or therapeutically treated with the small-molecule Gβγ inhibitor gallein. Tissue samples were analyzed by flow cytometry and immunohistochemistry. The development and extent of nephritis were assessed by monitoring proteinuria and by immunohistochemical analysis. Serum immunoglobulin levels were measured by enzyme-linked immunosorbent assay, and total IgG and anti-double-stranded DNA (anti-dsDNA) antibody-secreting cells were measured by enzyme-linked immunospot assay.Gallein inhibited accumulation of T cells and germinal center (GC) B cells in the spleen. Both prophylactic and therapeutic treatment reduced GC size, decreased antibody-secreting cell production in the spleen, and markedly decreased accumulation of autoreactive anti-dsDNA antibody-secreting cells in kidneys. Gallein also reduced immune complex deposition in kidneys. Finally, gallein treatment dramatically inhibited kidney inflammation, prevented glomerular damage, and decreased proteinuria. Mechanistically, gallein inhibited immune cell migration and signaling in response to chemokines in vitro, which suggests that its mechanisms of action in vivo are inhibition of migration of immune cells to sites of inflammation and inhibition of immune cell maturation.Overall, these data demonstrate the potential use of gallein or novel inhibitors of Gβγ signaling in SLE treatment.

Published
2016

16. Potassium conservation is impaired in mice with reduced renal expression of Kir4.1.

Author

Malik, Sundeep, Lambert, Emily, Junhui Zhang, Tong Wang, Clark, Heather L., Cypress, Michael, Goldman, Bruce I., Porter, George A., Pena, Salvador, Nino, Wilson, and Gray, Daniel A.

Subjects
POTASSIUM channels, PROTEIN expression, LABORATORY mice
Abstract

To better understand the role of the inward-rectifying K channel Kir4.1 (KCNJ10) in the distal nephron, we initially studied a global Kir4.1 knockout mouse (gKO), which demonstrated the hypokalemia and hypomagnesemia seen in SeSAME/EAST syndrome and was associated with reduced Na/Cl cotransporter (NCC) expression. Lethality by ~3 wk, however, limits the usefulness of this model, so we developed a kidney-specific Kir4.1 "knockdown" mouse (ksKD) using a cadherin 16 promoter and Cre-loxP methodology. These mice appeared normal and survived to adulthood. Kir4.1 protein expression was decreased ~50% vs. wild-type (WT) mice by immunoblotting, and immunofluorescence showed moderately reduced Kir4.1 staining in distal convoluted tubule that was minimal or absent in connecting tubule and cortical collecting duct. Under control conditions, the ksKD mice showed metabolic alkalosis and relative hypercalcemia but were normokalemic and mildly hypermagnesemic despite decreased NCC expression. In addition, the mice had a severe urinary concentrating defect associated with hypernatremia, enlarged kidneys with tubulocystic dilations, and reduced aquaporin-3 expression. On a K/Mg-free diet for 1 wk, however, ksKD mice showed marked hypokalemia (serum K: 1.5 ± 0.1 vs. 3.0 ± 0.1 mEq/l for WT), which was associated with renal K wasting (transtubular K gradient: 11.4 ± 0.8 vs. 1.6 ± 0.4 in WT). Phosphorylated-NCC expression increased in WT but not ksKD mice on the K/Mg-free diet, suggesting that loss of NCC adaptation underlies the hypokalemia. In conclusion, even modest reduction in Kir4.1 expression results in impaired K conservation, which appears to be mediated by reduced expression of activated NCC. [ABSTRACT FROM AUTHOR]

Published
2018
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17. Erratum: Beneficial effect of novel proteasome inhibitors in murine lupus via dual inhibition of type I interferon and autoantibody‐secreting cells

Author

Ichikawa, H. Travis, primary, Conley, Thomas, additional, Muchamuel, Tony, additional, Jiang, Jing, additional, Lee, Susan, additional, Owen, Teresa, additional, Barnard, Jennifer, additional, Nevarez, Sarah, additional, Goldman, Bruce I., additional, Kirk, Christopher J., additional, Looney, R. John, additional, and Anolik, Jennifer H., additional

Published
2012
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