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2. Macrophage-specific inhibition of the histone demethylase JMJD3 decreases STING and pathologic inflammation in diabetic wound repair

Author

Audu, Christopher O., Melvin, William J., Joshi, Amrita D., Wolf, Sonya J., Moon, Jadie Y., Davis, Frank M., Barrett, Emily C., Mangum, Kevin D., Deng, Hongping, Xing, Xianying, Wasikowski, Rachel, Tsoi, Lam C., Sharma, Sriganesh B., Bauer, Tyler M., Shadiow, James, Corriere, Matthew A., Obi, Andrea T., Kunkel, Steven L., Levi, Benjamin, Moore, Bethany B., Gudjonsson, Johann E., Smith, Andrew M., and Gallagher, Katherine A.

Published
2022
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3. Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2

Author

Melvin, William J., Audu, Christopher O., Davis, Frank M., Sharma, Sriganesh B., Joshi, Amrita, DenDekker, Aaron, Wolf, Sonya, Barrett, Emily, Mangum, Kevin, Zhou, Xiaofeng, Bame, Monica, Ruan, Alex, Obi, Andrea, Kunkel, Steven L., Moore, Bethany B., and Gallagher, Katherine A.

Published
2021

4. Diabetic Wound Keratinocytes Induce Macrophage JMJD3-Mediated Nlrp3 Expression via IL-1R Signaling.

Author

Wolf, Sonya J., Audu, Christopher O., Moon, Jadie Y., Joshi, Amrita D., Melvin, William J., Barrett, Emily C., Mangum, Kevin, de Jimenez, Gabriela Saldana, Rocco, Sabrina, Buckley, Sam, Ahmed, Zara, Wasikowski, Rachael, Kahlenberg, J. Michelle, Tsoi, Lam C., Gudjonsson, Johann E., and Gallagher, Katherine A.

Subjects
*MYELOID cells, *GENE expression, *WOUND healing, *NLRP3 protein, *TISSUE wounds
Abstract

Macrophage (Mφ) plasticity is critical for normal wound repair; however, in type 2 diabetic wounds, Mφs persist in a low-grade inflammatory state that prevents the resolution of wound inflammation. Increased NLRP3 inflammasome activity has been shown in diabetic wound Mφs; however, the molecular mechanisms regulating NLRP3 expression and activity are unclear. Here, we identified that diabetic wound keratinocytes induce Nlrp3 gene expression in wound Mφs through IL-1 receptor–mediated signaling, resulting in enhanced inflammasome activation in the presence of pathogen-associated molecular patterns and damage-associated molecular patterns. We found that IL-1α is increased in human and murine wound diabetic keratinocytes compared with nondiabetic controls and directly induces Mφ Nlrp3 expression through IL-1 receptor signaling. Mechanistically, we report that the histone demethylase, JMJD3, is increased in wound Mφs late post-injury and is induced by IL-1α from diabetic wound keratinocytes, resulting in Nlrp3 transcriptional activation through an H3K27me3-mediated mechanism. Using genetically engineered mice deficient in JMJD3 in myeloid cells (Jmjd3 f/f lyz2 Cre+), we demonstrate that JMJD3 controls Mφ-mediated Nlrp3 expression during diabetic wound healing. Thus, our data suggest a role for keratinocyte-mediated IL-1α/IL-1R signaling in driving enhanced NLRP3 inflammasome activity in wound Mφs. These data also highlight the importance of cell cross-talk in wound tissues and identify JMJD3 and the IL-1R signaling cascade as important upstream therapeutic targets for Mφ NLRP3 inflammasome hyperactivity in nonhealing diabetic wounds. Article Highlights: The molecular mechanism regulating macrophage (Mφ) NLRP3 inflammasome activity in diabetic wounds remains unclear. Diabetic wound keratinocytes induce Nlrp3 gene expression and enhance inflammasome activation in wound Mφs through IL-1 receptor–mediated signaling. IL-1α is increased in human and murine wound diabetic keratinocytes compared with nondiabetic controls and directly induces Mφ Nlrp3 expression via histone demethylase, JMJD3. JMJD3 controls Mφ-mediated Nlrp3 expression during wound healing. [ABSTRACT FROM AUTHOR]

Published
2024
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7. The histone methyltransferase Whsc1 regulates TGFβ-driven macrophage to myofibroblast transition

Author

Mangum, Kevin D, primary, Joshi, Amrita D, additional, Melvin, William J, additional, Mazumder, Purba, additional, Erturk, Asuman, additional, Wolf, Sonya, additional, Barrett, Emily C, additional, Moon, Jadie Yoonjoo, additional, Obi, Andrea, additional, Kunkel, Steven L, additional, Moore, Bethany B, additional, and Gallagher, Katherine, additional

Published
2023
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10. IL-17A-mediated JMJD3 regulation of integrin alpha 3 gene expression alters migration of diabetic keratinocytes and impairs wound repair.

Author

Moon, Jadie Yoonjoo, primary, Wolf, Sonya, additional, Audu, Christopher, additional, Melvin, William, additional, Joshi, Amrita, additional, Mangum, Kevin, additional, Barrett, Emily, additional, Davis, Frank, additional, Mazumder, Purba, additional, Rocco, Sabrina, additional, Erturk, Ilkim, additional, and Gallagher, Katherine, additional

Published
2023
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16. IFN-κ is critical for normal wound repair and is decreased in diabetic wounds

Author

Wolf, Sonya J., primary, Audu, Christopher O., additional, Joshi, Amrita, additional, denDekker, Aaron, additional, Melvin, William J., additional, Davis, Frank M., additional, Xing, Xianying, additional, Wasikowski, Rachael, additional, Tsoi, Lam C., additional, Kunkel, Steven L., additional, Gudjonsson, Johann E., additional, O’Riordan, Mary X., additional, Kahlenberg, J. Michelle, additional, and Gallagher, Katherine A., additional

Published
2022
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20. Interferon kappa (IFNk) in keratinocytes is critical for normal wound repair and is decreased in diabetic wounds

Author

Wolf, Sonya, primary, Audu, Christopher O, additional, Joshi, Amrita D, additional, denDekker, Aaron, additional, Melvin, William J., additional, Xing, Xianying, additional, Wasikowski, Rachael, additional, Tsoi, Lam C, additional, Gudjonsson, Johann E, additional, Kahlenberg, J Michelle, additional, and Gallagher, Katherine A, additional

Published
2022
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25. Inhibition of macrophage histone demethylase JMJD3 protects against abdominal aortic aneurysms

Author

Davis, Frank M., primary, Tsoi, Lam C., additional, Melvin, William J., additional, denDekker, Aaron, additional, Wasikowski, Rachael, additional, Joshi, Amrita D., additional, Wolf, Sonya, additional, Obi, Andrea T., additional, Billi, Allison C., additional, Xing, Xianying, additional, Audu, Christopher, additional, Moore, Bethany B., additional, Kunkel, Steven L., additional, Daugherty, Alan, additional, Lu, Hong S., additional, Gudjonsson, Johann E., additional, and Gallagher, Katherine A., additional

Published
2021
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27. Epigenetic regulation of the PGE2 pathway modulates macrophage phenotype in normal and pathologic wound repair

Author

Davis, Frank M., primary, Tsoi, Lam C., additional, Wasikowski, Rachael, additional, denDekker, Aaron, additional, Joshi, Amrita, additional, Wilke, Carol, additional, Deng, Hongping, additional, Wolf, Sonya, additional, Obi, Andrea, additional, Huang, Steven, additional, Billi, Allison C., additional, Robinson, Scott, additional, Lipinski, Jay, additional, Melvin, William J., additional, Audu, Christopher O., additional, Weidinger, Stephan, additional, Kunkel, Steven L., additional, Smith, Andrew, additional, Gudjonsson, Johann E., additional, Moore, Bethany B., additional, and Gallagher, Katherine A., additional

Published
2020
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30. Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair

Author

Davis, Frank M., primary, denDekker, Aaron, additional, Kimball, Andrew, additional, Joshi, Amrita D., additional, El Azzouny, Mahmoud, additional, Wolf, Sonya J., additional, Obi, Andrea T., additional, Lipinski, Jay, additional, Gudjonsson, Johann E., additional, Xing, Xianying, additional, Plazyo, Olesya, additional, Audu, Christopher, additional, Melvin, William J., additional, Singer, Kanakadurga, additional, Henke, Peter K., additional, Moore, Bethany B., additional, Burant, Charles, additional, Kunkel, Steven L., additional, and Gallagher, Katherine A., additional

Published
2020
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31. TNF-α regulates diabetic macrophage function through the histone acetyltransferase MOF

Author

denDekker, Aaron D., primary, Davis, Frank M., additional, Joshi, Amrita D., additional, Wolf, Sonya J., additional, Allen, Ronald, additional, Lipinski, Jay, additional, Nguyen, Brenda, additional, Kirma, Joseph, additional, Nycz, Dylan, additional, Bermick, Jennifer, additional, Moore, Bethany B., additional, Gudjonsson, Johann E., additional, Kunkel, Steven L., additional, and Gallagher, Katherine A., additional

Published
2020
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33. The female-biased factor VGLL3 drives cutaneous and systemic autoimmunity

Author

Billi, Allison C., primary, Gharaee-Kermani, Mehrnaz, additional, Fullmer, Joseph, additional, Tsoi, Lam C., additional, Hill, Brett D., additional, Gruszka, Dennis, additional, Ludwig, Jessica, additional, Xing, Xianying, additional, Estadt, Shannon, additional, Wolf, Sonya J., additional, Rizvi, Syed Monem, additional, Berthier, Celine C., additional, Hodgin, Jeffrey B., additional, Beamer, Maria A., additional, Sarkar, Mrinal K., additional, Liang, Yun, additional, Uppala, Ranjitha, additional, Shao, Shuai, additional, Zeng, Chang, additional, Harms, Paul W., additional, Verhaegen, Monique E., additional, Voorhees, John J., additional, Wen, Fei, additional, Ward, Nicole L., additional, Dlugosz, Andrzej A., additional, Kahlenberg, J. Michelle, additional, and Gudjonsson, Johann E., additional

Published
2019
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39. IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation

Author

Gharaee-Kermani, Mehrnaz, Estadt, Shannon N., Tsoi, Lam C., Wolf, Sonya J., Liu, Jianhua, Xing, Xianying, Theros, Jonathon, Reed, Tammi J., Lowe, Lori, Gruszka, Dennis, Ward, Nicole L., Gudjonsson, Johann E., and Kahlenberg, J. Michelle

Abstract

Psoriasis is a common, inflammatory autoimmune skin disease. Early detection of an IFN-1 signature occurs in many psoriasis lesions, but the source of IFN production remains debated. IFN-κ is an important source of IFN-1 production in the epidermis. We identified a correlation between IFN-regulated and psoriasis-associated genes in human lesional skin. We thus wanted to explore the effects of IFN-κ in psoriasis using the well-characterized imiquimod psoriasis model. Three mouse strains aged 10 weeks were used: wild-type C57Bl/6, C57Bl/6 that overexpress Ifnkin the epidermis (i.e., transgenic), and total body Ifnk–/–(i.e., knockout) strain. Psoriasis was induced by topical application of imiquimod on both ears for 8 consecutive days. Notably, the severity of skin lesions and inflammatory cell infiltration was more significantly increased in transgenic than in wild-type than in knockout mice. Gene expression analysis identified a more upregulation of Mxa, Il1b, Tnfa, Il6, Il12, Il23, Il17,and Ifngin transgenic than in wild-type than in knockout mice after imiquimod treatment. Furthermore, imiquimod increased CD8+and CD4+T-cell infiltration more in transgenic than in wild-type than in knockout mice. In summary, we identified IFN-κ as a rheostat for initiation of psoriasiform inflammation. This suggests that targeting IFN-1s early in the disease may be an effective way of controlling psoriatic inflammation.

Published
2021
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40. The histone methyltransferase mixed-lineage-leukemia-1 drives T cell phenotype via notch signaling in diabetic tissue repair.

Author

Melvin WJ, Bauer TM, Magnum KD, Audu CO, Shadiow J, Barrett E, Joshi A, Moon JY, Bogel R, Mazumder P, Wolf SJ, Kunkel S, Gudjonsson JE, Davis FM, and Gallagher KA

Abstract

Immune cell mediated inflammation is important in normal tissue regeneration but can be pathologic in diabetic wounds. Limited literature exists on the role of CD4+T cells in normal or diabetic wound repair, however, the imbalance of CD4+TH17/Treg cells has been found to promote inflammation in other diabetic tissues. Here, using human tissue and murine transgenic models, we identified that the histone methyltransferase MLL1 directly regulates the TH17 transcription factor RORγ via an H3K4me3 mechanism and increases expression of Notch receptors and downstream Notch signaling. Further, we found that Notch receptor signaling regulates CD4+TH cell differentiation and is critical for normal wound repair, and loss of upstream Notch pathway mediators or receptors in CD4+T cells resulted in the loss of CD4+TH cell differentiation in wounds. In diabetes, MLL1 and Notch-receptor signaling were upregulated in wound CD4+TH cells, driving CD4+ T cells towards the TH17 cell phenotype. Treatment of diabetic wound CD4T cells with a small molecule inhibitor of MLL1 (MI-2) yielded a significant reduction in CD4+TH17 cells and IL17A. This is the first study to identify the MLL1-mediated mechanisms responsible for regulating the TH17/Treg balance in normal and diabetic wounds and define the complex role of Notch signaling in CD4+T cells in wounds, where increased or decreased Notch signaling both result in pathologic wound repair. Therapeutic targeting of MLL1 in diabetic CD4+TH cells may decrease pathologic inflammation through regulation of CD4+T cell differentiation.

Published
2024
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41. Epigenetic Alteration of Smooth Muscle Cells Regulates Endothelin-Dependent Blood Pressure and Hypertensive Arterial Remodeling.

Author

Mangum KD, Li Q, Bauer TM, Wolf SJ, Shadiow J, Moon JY, Barrett EC, Joshi AD, Ahmed Z, Wasikowski R, Boyer K, Obi AT, Davis FM, Chang L, Tsoi LC, Gudjonsson J, and Gallagher KA

Abstract

Long-standing hypertension (HTN) affects multiple organ systems and leads to pathologic arterial remodeling, which is driven largely by smooth muscle cell (SMC) plasticity. Although genome wide association studies (GWAS) have identified numerous variants associated with changes in blood pressure in humans, only a small percentage of these variants actually cause HTN. In order to identify relevant genes important in SMC function in HTN, we screened three separate human GWAS and Mendelian randomization studies to identify SNPs located within non-coding gene regions, focusing on genes encoding epigenetic enzymes, as these have been recently identified to control SMC fate in cardiovascular disease. We identified SNPs rs62059712 and rs74480102 in the promoter of the human JMJD3 gene and show that the minor C allele increases JMJD3 transcription in SMCs via increased SP1 binding to the JMJD3 promoter. Using our novel SMC-specific Jmjd3-deficient murine model ( Jmjd3 flox/flox Myh11 CreERT ), we show that loss of Jmjd3 in SMCs results in HTN, mechanistically, due to decreased EDNRB expression and a compensatory increase in EDNRA expression. As a translational corollary, through single cell RNA-sequencing (scRNA-seq) of human arteries, we found strong correlation between JMJD3 and EDNRB expression in SMCs. Further, we identified that JMJD3 is required for SMC-specific gene expression, and loss of JMJD3 in SMCs in the setting of HTN results in increased arterial remodeling by promoting the SMC synthetic phenotype. Our findings link a HTN-associated human DNA variant with regulation of SMC plasticity, revealing therapeutic targets that may be used in the screening and/or personalized treatment of HTN.

Published
2024
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42. Histone demethylase JARID1C/KDM5C regulates Th17 cells by increasing IL-6 expression in diabetic plasmacytoid dendritic cells.

Author

Audu CO, Wolf SJ, Joshi AD, Moon JY, Melvin WJ, Sharma SB, Davis FM, Obi AT, Wasikowski R, Tsoi LC, Barrett EC, Mangum KD, Bauer TM, Kunkel SL, Moore BB, and Gallagher KA

Subjects
Animals, Female, Humans, Male, Mice, Interleukin-17 metabolism, Jumonji Domain-Containing Histone Demethylases metabolism, Jumonji Domain-Containing Histone Demethylases genetics, Mice, Inbred C57BL, Dendritic Cells immunology, Dendritic Cells metabolism, Interleukin-6 metabolism, Th17 Cells immunology, Th17 Cells metabolism, Wound Healing immunology
Abstract

Plasmacytoid dendritic cells (pDCs) are first responders to tissue injury, where they prime naive T cells. The role of pDCs in physiologic wound repair has been examined, but little is known about pDCs in diabetic wound tissue and their interactions with naive CD4+ T cells. Diabetic wounds are characterized by increased levels of inflammatory IL-17A cytokine, partly due to increased Th17 CD4+ cells. This increased IL-17A cytokine, in excess, impairs tissue repair. Here, using human tissue and murine wound healing models, we found that diabetic wound pDCs produced excess IL-6 and TGF-β and that these cytokines skewed naive CD4+ T cells toward a Th17 inflammatory phenotype following cutaneous injury. Further, we identified that increased IL-6 cytokine production by diabetic wound pDCs is regulated by a histone demethylase, Jumonji AT-rich interactive domain 1C histone demethylase (JARID1C). Decreased JARID1C increased IL-6 transcription in diabetic pDCs, and this process was regulated upstream by an IFN-I/TYK2/JAK1,3 signaling pathway. When inhibited in nondiabetic wound pDCs, JARID1C skewed naive CD4+ T cells toward a Th17 phenotype and increased IL-17A production. Together, this suggests that diabetic wound pDCs are epigenetically altered to increase IL-6 expression that then affects T cell phenotype. These findings identify a therapeutically manipulable pathway in diabetic wounds.

Published
2024
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