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Article ; Online: HDAC11 inhibition triggers bimodal thermogenic pathways to circumvent adipocyte catecholamine resistance.

Robinson, Emma L / Bagchi, Rushita A / Major, Jennifer L / Bergman, Bryan C / Matsuda, Jennifer L / McKinsey, Timothy A

2023 Volume 133, Issue 19

Abstract: Stimulation of adipocyte β-adrenergic receptors (β-ARs) induces expression of uncoupling protein 1 (UCP1), promoting nonshivering thermogenesis. Association of β-ARs with a lysine-myristoylated form of A kinase-anchoring protein 12 (AKAP12, also known as ...

Abstract	Stimulation of adipocyte β-adrenergic receptors (β-ARs) induces expression of uncoupling protein 1 (UCP1), promoting nonshivering thermogenesis. Association of β-ARs with a lysine-myristoylated form of A kinase-anchoring protein 12 (AKAP12, also known as gravin-α) is required for downstream signaling that culminates in UCP1 induction. Conversely, demyristoylation of gravin-α by histone deacetylase 11 (HDAC11) suppresses this pathway. Whether inhibition of HDAC11 in adipocytes is sufficient to drive UCP1 expression independently of β-ARs is not known. Here, we demonstrate that adipocyte-specific deletion of HDAC11 in mice leads to robust induction of UCP1 in adipose tissue (AT), resulting in increased body temperature. These effects are mimicked by treating mice in vivo or human AT ex vivo with an HDAC11-selective inhibitor, FT895. FT895 triggers biphasic, gravin-α myristoylation-dependent induction of UCP1 protein expression, with a noncanonical acute response that is posttranscriptional and independent of protein kinase A (PKA), and a delayed response requiring PKA activity and new Ucp1 mRNA synthesis. Remarkably, HDAC11 inhibition promotes UCP1 expression even in models of adipocyte catecholamine resistance where β-AR signaling is blocked. These findings define cell-autonomous, multimodal roles for HDAC11 as a suppressor of thermogenesis, and highlight the potential of inhibiting HDAC11 to therapeutically alter AT phenotype independently of β-AR stimulation.
MeSH term(s)	Animals ; Humans ; Mice ; Adipocytes/drug effects ; Adipocytes/metabolism ; Adipose Tissue/metabolism ; Adipose Tissue, Brown/metabolism ; Catecholamines/pharmacology ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Thermogenesis/genetics ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism ; Histone Deacetylase Inhibitors/pharmacology
Chemical Substances	Catecholamines ; HDAC11 protein, human (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98) ; Uncoupling Protein 1 ; Histone Deacetylase Inhibitors
Language	English
Publishing date	2023-10-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI168192
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Article ; Online: HDAC11 inhibition triggers bimodal thermogenic pathways to circumvent adipocyte catecholamine resistance

Emma L. Robinson / Rushita A. Bagchi / Jennifer L. Major / Bryan C. Bergman / Jennifer L. Matsuda / Timothy A. McKinsey

The Journal of Clinical Investigation, Vol 133, Iss

2023 Volume 19

Abstract	Stimulation of adipocyte β-adrenergic receptors (β-ARs) induces expression of uncoupling protein 1 (UCP1), promoting nonshivering thermogenesis. Association of β-ARs with a lysine-myristoylated form of A kinase–anchoring protein 12 (AKAP12, also known as gravin-α) is required for downstream signaling that culminates in UCP1 induction. Conversely, demyristoylation of gravin-α by histone deacetylase 11 (HDAC11) suppresses this pathway. Whether inhibition of HDAC11 in adipocytes is sufficient to drive UCP1 expression independently of β-ARs is not known. Here, we demonstrate that adipocyte-specific deletion of HDAC11 in mice leads to robust induction of UCP1 in adipose tissue (AT), resulting in increased body temperature. These effects are mimicked by treating mice in vivo or human AT ex vivo with an HDAC11-selective inhibitor, FT895. FT895 triggers biphasic, gravin-α myristoylation–dependent induction of UCP1 protein expression, with a noncanonical acute response that is posttranscriptional and independent of protein kinase A (PKA), and a delayed response requiring PKA activity and new Ucp1 mRNA synthesis. Remarkably, HDAC11 inhibition promotes UCP1 expression even in models of adipocyte catecholamine resistance where β-AR signaling is blocked. These findings define cell-autonomous, multimodal roles for HDAC11 as a suppressor of thermogenesis, and highlight the potential of inhibiting HDAC11 to therapeutically alter AT phenotype independently of β-AR stimulation.
Keywords	Metabolism ; Medicine ; R
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A Distinctive γδ T Cell Repertoire in NOD Mice Weakens Immune Regulation and Favors Diabetic Disease.

O'Brien, Rebecca L / Matsuda, Jennifer / Aydintug, M Kemal / Jin, Niyun / Phalke, Swati / Born, Willi K

Biomolecules

2022 Volume 12, Issue 10

Abstract: Previous studies in mice and humans suggesting that ... γδ ... T cells play a role in the development of type 1 diabetes have been inconsistent and contradictory. We attempted to resolve this for the type 1 diabetes-prone NOD mice by characterizing their < ...

Abstract	Previous studies in mice and humans suggesting that γδ T cells play a role in the development of type 1 diabetes have been inconsistent and contradictory. We attempted to resolve this for the type 1 diabetes-prone NOD mice by characterizing their γδ T cell populations, and by investigating the functional contributions of particular γδ T cells subsets, using Vγ-gene targeted NOD mice. We found evidence that NOD Vγ4+ γδ T cells inhibit the development of diabetes, and that the process by which they do so involves IL-17 production and/or promotion of regulatory CD4+ αβ T cells (Tregs) in the pancreatic lymph nodes. In contrast, the NOD Vγ1+ cells promote diabetes development. Enhanced Vγ1+ cell numbers in NOD mice, in particular those biased to produce IFNγ, appear to favor diabetic disease. Within NOD mice deficient in particular γδ T cell subsets, we noted that changes in the abundance of non-targeted T cell types also occurred, which varied depending upon the γδ T cells that were missing. Our results indicate that while certain γδ T cell subsets inhibit the development of spontaneous type 1 diabetes, others exacerbate it, and they may do so via mechanisms that include altering the levels of other T cells.
MeSH term(s)	Mice ; Humans ; Animals ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Mice, Inbred NOD ; Interleukin-17/metabolism ; Diabetes Mellitus, Type 1/metabolism ; T-Lymphocyte Subsets ; Mice, Inbred C57BL
Chemical Substances	Receptors, Antigen, T-Cell, gamma-delta ; Interleukin-17
Language	English
Publishing date	2022-10-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12101406
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Article ; Online: Myeloid Cell CK2 Regulates Inflammation and Resistance to Bacterial Infection.

Larson, Sandy R / Bortell, Nikki / Illies, Alysha / Crisler, William J / Matsuda, Jennifer L / Lenz, Laurel L

Frontiers in immunology

2020 Volume 11, Page(s) 590266

Abstract: Kinase activity plays an essential role in the regulation of immune cell defenses against pathogens. The protein kinase CK2 (formerly casein kinase II) is an evolutionarily conserved kinase with hundreds of identified substrates. CK2 is ubiquitously ... ...

Abstract	Kinase activity plays an essential role in the regulation of immune cell defenses against pathogens. The protein kinase CK2 (formerly casein kinase II) is an evolutionarily conserved kinase with hundreds of identified substrates. CK2 is ubiquitously expressed in somatic and immune cells, but the roles of CK2 in regulation of immune cell function remain largely elusive. This reflects the essential role of CK2 in organismal development and limited prior work with conditional CK2 mutant murine models. Here, we generated mice with a conditional (floxed) allele of
MeSH term(s)	Animals ; Casein Kinase II/genetics ; Casein Kinase II/immunology ; Female ; Inflammation/immunology ; Listeria monocytogenes ; Listeriosis/immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/immunology
Chemical Substances	Casein Kinase II (EC 2.7.11.1)
Language	English
Publishing date	2020-12-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.590266
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Article ; Online: Iloprost requires the Frizzled-9 receptor to prevent lung cancer.

Sompel, Kayla / Dwyer-Nield, Lori D / Smith, Alex J / Elango, Alamelu / Backos, Don S / Zhang, Bicheng / Gross, James / Ternyak, Kristina / Matsuda, Jennifer L / Kopf, Katrina / Keith, Robert L / Tennis, Meredith A

iScience

2022 Volume 25, Issue 6, Page(s) 104442

Abstract: Prevention of premalignant lesion progression is a promising approach to reducing lung cancer burden in high-risk populations. Substantial preclinical and clinical evidence has demonstrated efficacy of the prostacyclin analogue iloprost for lung cancer ... ...

Abstract	Prevention of premalignant lesion progression is a promising approach to reducing lung cancer burden in high-risk populations. Substantial preclinical and clinical evidence has demonstrated efficacy of the prostacyclin analogue iloprost for lung cancer chemoprevention. Iloprost activates peroxisome proliferator-activated receptor gamma (PPARG) to initiate chemopreventive signaling and
Language	English
Publishing date	2022-05-23
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.104442
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Role of a "Magic" Methyl: 2'-Deoxy-2'-α-F-2'-β-

Guenther, Dale C / Mori, Shohei / Matsuda, Shigeo / Gilbert, Jason A / Willoughby, Jennifer L S / Hyde, Sarah / Bisbe, Anna / Jiang, Yongfeng / Agarwal, Saket / Madaoui, Mimouna / Janas, Maja M / Charisse, Klaus / Maier, Martin A / Egli, Martin / Manoharan, Muthiah

Journal of the American Chemical Society

2022 Volume 144, Issue 32, Page(s) 14517–14534

Abstract: Although 2'-deoxy-2'-α-F-2'-β- ...

Abstract	Although 2'-deoxy-2'-α-F-2'-β-
MeSH term(s)	Animals ; Liposomes ; Mice ; Models, Molecular ; Nanoparticles ; Nucleic Acid Conformation ; Nucleosides ; Nucleotides ; Oligonucleotides ; Organophosphonates ; Phosphates ; Pyrimidine Nucleotides ; RNA Interference ; RNA, Small Interfering/genetics
Chemical Substances	Lipid Nanoparticles ; Liposomes ; Nucleosides ; Nucleotides ; Oligonucleotides ; Organophosphonates ; Phosphates ; Pyrimidine Nucleotides ; RNA, Small Interfering
Language	English
Publishing date	2022-08-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	3155-0
ISSN	1520-5126 ; 0002-7863
ISSN (online)	1520-5126
ISSN	0002-7863
DOI	10.1021/jacs.2c01679
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Article ; Online: Iloprost requires the Frizzled-9 receptor to prevent lung cancer

Kayla Sompel / Lori D. Dwyer-Nield / Alex J. Smith / Alamelu Elango / Don S. Backos / Bicheng Zhang / James Gross / Kristina Ternyak / Jennifer L. Matsuda / Katrina Kopf / Robert L. Keith / Meredith A. Tennis

iScience, Vol 25, Iss 6, Pp 104442- (2022)

2022

Abstract: Summary: Prevention of premalignant lesion progression is a promising approach to reducing lung cancer burden in high-risk populations. Substantial preclinical and clinical evidence has demonstrated efficacy of the prostacyclin analogue iloprost for lung ...

Abstract	Summary: Prevention of premalignant lesion progression is a promising approach to reducing lung cancer burden in high-risk populations. Substantial preclinical and clinical evidence has demonstrated efficacy of the prostacyclin analogue iloprost for lung cancer chemoprevention. Iloprost activates peroxisome proliferator-activated receptor gamma (PPARG) to initiate chemopreventive signaling and in vitro, which requires the transmembrane receptor Frizzled9 (FZD9). We hypothesized a Fzd9−/− mouse would not be protected by iloprost in a lung cancer model. Fzd9−/− mice were treated with inhaled iloprost in a urethane model of lung adenoma. We found that Fzd9−/− mice treated with iloprost were not protected from adenoma development compared to wild-type mice nor did they demonstrate increased activation of iloprost signaling pathways. Our results established that iloprost requires FZD9 in vivo for lung cancer chemoprevention. This work represents a critical advancement in defining iloprost’s chemopreventive mechanisms and identifies a potential response marker for future clinical trials.
Keywords	Biological sciences ; Biochemistry ; Cancer ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metabolically Stable Anomeric Linkages Containing GalNAc-siRNA Conjugates: An Interplay among ASGPR, Glycosidase, and RISC Pathways.

Kandasamy, Pachamuthu / Mori, Shohei / Matsuda, Shigeo / Erande, Namrata / Datta, Dhrubajyoti / Willoughby, Jennifer L S / Taneja, Nate / O'Shea, Jonathan / Bisbe, Anna / Manoharan, Rajar M / Yucius, Kristina / Nguyen, Tuyen / Indrakanti, Ramesh / Gupta, Swati / Gilbert, Jason A / Racie, Tim / Chan, Amy / Liu, Ju / Hutabarat, Renta /

Nair, Jayaprakash K / Charisse, Klaus / Maier, Martin A / Rajeev, Kallanthottathil G / Egli, Martin / Manoharan, Muthiah

Journal of medicinal chemistry

2023 Volume 66, Issue 4, Page(s) 2506–2523

Abstract: Conjugation of synthetic ... ...

Abstract	Conjugation of synthetic triantennary
MeSH term(s)	Animals ; Mice ; Acetylgalactosamine/chemistry ; Asialoglycoprotein Receptor/metabolism ; Galactosamine ; Glycoside Hydrolases/metabolism ; Glycosides/metabolism ; Hepatocytes/metabolism ; Ligands ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/metabolism
Chemical Substances	Acetylgalactosamine (KM15WK8O5T) ; Asialoglycoprotein Receptor ; Galactosamine (7535-00-4) ; Glycoside Hydrolases (EC 3.2.1.-) ; Glycosides ; Ligands ; RNA, Small Interfering ; RNA-Induced Silencing Complex
Language	English
Publishing date	2023-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.2c01337
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Zs.B 151: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Anaerobic respiration of host-derived methionine sulfoxide protects intracellular Salmonella from the phagocyte NADPH oxidase.

Kim, Ju-Sim / Liu, Lin / Kant, Sashi / Orlicky, David J / Uppalapati, Siva / Margolis, Alyssa / Davenport, Bennett J / Morrison, Thomas E / Matsuda, Jennifer / McClelland, Michael / Jones-Carson, Jessica / Vazquez-Torres, Andres

Cell host & microbe

2024 Volume 32, Issue 3, Page(s) 411–424.e10

Abstract: Intracellular Salmonella experiencing oxidative stress downregulates aerobic respiration. To maintain cellular energetics during periods of oxidative stress, intracellular Salmonella must utilize terminal electron acceptors of lower energetic value than ... ...

Abstract	Intracellular Salmonella experiencing oxidative stress downregulates aerobic respiration. To maintain cellular energetics during periods of oxidative stress, intracellular Salmonella must utilize terminal electron acceptors of lower energetic value than molecular oxygen. We show here that intracellular Salmonella undergoes anaerobic respiration during adaptation to the respiratory burst of the phagocyte NADPH oxidase in macrophages and in mice. Reactive oxygen species generated by phagocytes oxidize methionine, generating methionine sulfoxide. Anaerobic Salmonella uses the molybdenum cofactor-containing DmsABC enzymatic complex to reduce methionine sulfoxide. The enzymatic activity of the methionine sulfoxide reductase DmsABC helps Salmonella maintain an alkaline cytoplasm that supports the synthesis of the antioxidant hydrogen sulfide via cysteine desulfuration while providing a source of methionine and fostering redox balancing by associated dehydrogenases. Our investigations demonstrate that nontyphoidal Salmonella responding to oxidative stress exploits the anaerobic metabolism associated with dmsABC gene products, a pathway that has accrued inactivating mutations in human-adapted typhoidal serovars.
MeSH term(s)	Animals ; Mice ; Humans ; NADPH Oxidases ; Anaerobiosis ; Phagocytes/metabolism ; Methionine/metabolism ; Methionine/analogs & derivatives ; Salmonella typhimurium/metabolism ; Respiration
Chemical Substances	NADPH Oxidases (EC 1.6.3.-) ; methionine sulfoxide (XN1XVI4B2C) ; Methionine (AE28F7PNPL)
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2024.01.004
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Article ; Online: Coral bleaching response is unaltered following acclimatization to reefs with distinct environmental conditions.

Barott, Katie L / Huffmyer, Ariana S / Davidson, Jennifer M / Lenz, Elizabeth A / Matsuda, Shayle B / Hancock, Joshua R / Innis, Teegan / Drury, Crawford / Putnam, Hollie M / Gates, Ruth D

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 22

Abstract: Urgent action is needed to prevent the demise of coral reefs as the climate crisis leads to an increasingly warmer and more acidic ocean. Propagating climate change-resistant corals to restore degraded reefs is one promising strategy; however, empirical ... ...

Abstract	Urgent action is needed to prevent the demise of coral reefs as the climate crisis leads to an increasingly warmer and more acidic ocean. Propagating climate change-resistant corals to restore degraded reefs is one promising strategy; however, empirical evidence is needed to determine whether stress resistance is affected by transplantation beyond a coral's native reef. Here, we assessed the performance of bleaching-resistant individuals of two coral species following reciprocal transplantation between reefs with distinct pH, salinity, dissolved oxygen, sedimentation, and flow dynamics to determine whether heat stress response is altered following coral exposure to novel physicochemical conditions in situ. Critically, transplantation had no influence on coral heat stress responses, indicating that this trait was relatively fixed. In contrast, growth was highly plastic, and native performance was not predictive of performance in the novel environment. Coral metabolic rates and overall fitness were higher at the reef with higher flow, salinity, sedimentation, and diel fluctuations of pH and dissolved oxygen, and did not differ between native and cross-transplanted corals, indicating acclimatization via plasticity within just 3 mo. Conversely, cross-transplants at the second reef had higher fitness than native corals, thus increasing the fitness potential of the recipient population. This experiment was conducted during a nonbleaching year, so the potential benefits to recipient population fitness are likely enhanced during bleaching years. In summary, this study demonstrates that outplanting bleaching-resistant corals is a promising tool for elevating the resistance of coral populations to ocean warming.
MeSH term(s)	Acclimatization ; Animals ; Anthozoa/physiology ; Climate Change ; Coral Reefs ; Heat-Shock Response
Language	English
Publishing date	2021-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2025435118
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