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Article ; Online: Not all fiber is good for you: targeting fibroblast activation to improve cardiac function in heart failure.

Haushalter, Kristofer J / Patel, Hemal H

American journal of physiology. Heart and circulatory physiology

2018 Volume 315, Issue 4, Page(s) H1000–H1001

MeSH term(s)	Fibroblasts ; Heart Failure ; Humans ; Myocardium ; Ventricular Remodeling
Language	English
Publishing date	2018-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00386.2018
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Article ; Online: Multiplex Flow Assays

Kristofer J. Haushalter / Srinivas Vetcha / Robert C. Haushalter

ACS Omega, Vol 1, Iss 4, Pp 586-

2016 Volume 599

Keywords	Chemistry ; QD1-999
Language	English
Publishing date	2016-10-01T00:00:00Z
Publisher	American Chemical Society
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Multiplex Flow Assays.

Haushalter, Kristofer J / Vetcha, Srinivas / Haushalter, Robert C

ACS omega

2016 Volume 1, Issue 4, Page(s) 586–599

Abstract: Lateral flow or dipstick assays (e.g., home pregnancy tests), where an analyte solution is drawn through a porous membrane and is detected by localization onto a capture probe residing at a specific site on the flow strip, are the most commonly and ... ...

Abstract	Lateral flow or dipstick assays (e.g., home pregnancy tests), where an analyte solution is drawn through a porous membrane and is detected by localization onto a capture probe residing at a specific site on the flow strip, are the most commonly and extensively used type of diagnostic assay. However, after over 30 years of use, these assays are constrained to measuring one or a few analytes at a time. Here, we describe a completely general method, in which any single-plex lateral flow assay is transformed into a multiplex assay capable of measuring an arbitrarily large number of analytes simultaneously. Instead of identifying the analyte by its localization onto a specific geometric location in the flow medium, the analyte-specific capture probe is identified by its association with a specific optically encoded region within the flow medium. The capture probes for nucleic acids, antigens, or antibodies are attached to highly porous agarose beads, which have been encoded using multiple lanthanide emitters to create a unique optical signature for each capture probe. The optically encoded capture probe-derivatized beads are placed in contact with the analyte-containing porous flow medium and the analytes are captured onto the encoded regions as the solution flows through the porous medium. To perform a multiplex diagnostic assay, a solution comprising multiple analytes is passed through the flow medium containing the capture probe-derivatized beads, and the captured analyte is treated with a suitable fluorescent reporter. We demonstrate this multiplex analysis technique by simultaneously measuring DNA samples, antigen-antibody pairs, and mixtures of multiple nucleic acids and antibodies.
Language	English
Publishing date	2016-10-17
Publishing country	United States
Document type	Journal Article
ISSN	2470-1343
ISSN	2470-1343
DOI	10.1021/acsomega.6b00188
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Article ; Online: Phosphorylation of protein kinase A (PKA) regulatory subunit RIα by protein kinase G (PKG) primes PKA for catalytic activity in cells.

Haushalter, Kristofer J / Casteel, Darren E / Raffeiner, Andrea / Stefan, Eduard / Patel, Hemal H / Taylor, Susan S

The Journal of biological chemistry

2018 Volume 293, Issue 12, Page(s) 4411–4421

Abstract: cAMP-dependent protein kinase (PKAc) is a pivotal signaling protein in eukaryotic cells. PKAc has two well-characterized regulatory subunit proteins, RI and RII (each having α and β isoforms), which keep the PKAc catalytic subunit in a catalytically ... ...

Abstract	cAMP-dependent protein kinase (PKAc) is a pivotal signaling protein in eukaryotic cells. PKAc has two well-characterized regulatory subunit proteins, RI and RII (each having α and β isoforms), which keep the PKAc catalytic subunit in a catalytically inactive state until activation by cAMP. Previous reports showed that the RIα regulatory subunit is phosphorylated by cGMP-dependent protein kinase (PKG)
MeSH term(s)	Binding Sites ; Catalytic Domain ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/genetics ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/metabolism ; Cyclic GMP-Dependent Protein Kinases/genetics ; Cyclic GMP-Dependent Protein Kinases/metabolism ; HEK293 Cells ; Humans ; Phosphorylation ; Protein Binding
Chemical Substances	Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Cyclic AMP (E0399OZS9N) ; Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12)
Language	English
Publishing date	2018-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M117.809988
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Article ; Online: Intratumoral immunotherapy using platelet-cloaked nanoparticles enhances antitumor immunity in solid tumors.

Bahmani, Baharak / Gong, Hua / Luk, Brian T / Haushalter, Kristofer J / DeTeresa, Ethel / Previti, Mark / Zhou, Jiarong / Gao, Weiwei / Bui, Jack D / Zhang, Liangfang / Fang, Ronnie H / Zhang, Jie

Nature communications

2021 Volume 12, Issue 1, Page(s) 1999

Abstract: Intratumoral immunotherapy is an emerging modality for the treatment of solid tumors. Toll-like receptor (TLR) agonists have shown promise for eliciting immune responses, but systemic administration often results in the development of adverse side ... ...

Abstract	Intratumoral immunotherapy is an emerging modality for the treatment of solid tumors. Toll-like receptor (TLR) agonists have shown promise for eliciting immune responses, but systemic administration often results in the development of adverse side effects. Herein, we investigate whether localized delivery of the TLR agonist, resiquimod (R848), via platelet membrane-coated nanoparticles (PNP-R848) elicits antitumor responses. The membrane coating provides a means of enhancing interactions with the tumor microenvironment, thereby maximizing the activity of R848. Intratumoral administration of PNP-R848 strongly enhances local immune activation and leads to complete tumor regression in a colorectal tumor model, while providing protection against repeated tumor re-challenges. Moreover, treatment of an aggressive breast cancer model with intratumoral PNP-R848 delays tumor growth and inhibits lung metastasis. Our findings highlight the promise of locally delivering immunostimulatory payloads using biomimetic nanocarriers, which possess advantages such as enhanced biocompatibility and natural targeting affinities.
MeSH term(s)	Animals ; Blood Platelets/chemistry ; Blood Platelets/metabolism ; Breast Neoplasms/immunology ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Cell Line, Tumor ; Cell Membrane/chemistry ; Cell Membrane/metabolism ; Cells, Cultured ; Female ; HT29 Cells ; Humans ; Imidazoles/chemistry ; Imidazoles/immunology ; Imidazoles/therapeutic use ; Immunotherapy/methods ; Lung Neoplasms/immunology ; Lung Neoplasms/prevention & control ; Lung Neoplasms/secondary ; Mice, Inbred C57BL ; Nanoparticles/chemistry ; Nanoparticles/therapeutic use ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Treatment Outcome ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology ; Mice
Chemical Substances	Imidazoles ; resiquimod (V3DMU7PVXF)
Language	English
Publishing date	2021-03-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-22311-z
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Article ; Online: Intratumoral immunotherapy using platelet-cloaked nanoparticles enhances antitumor immunity in solid tumors

Baharak Bahmani / Hua Gong / Brian T. Luk / Kristofer J. Haushalter / Ethel DeTeresa / Mark Previti / Jiarong Zhou / Weiwei Gao / Jack D. Bui / Liangfang Zhang / Ronnie H. Fang / Jie Zhang

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 12

Abstract: The immunostimulatory properties of TLR7/8 agonists, such as resiquimod, have been exploited for cancer immunotherapy. Here, the authors design platelet membrane-cloaked nanoparticles for selective intratumoral delivery of resiquimod, resulting in potent ...

Abstract	The immunostimulatory properties of TLR7/8 agonists, such as resiquimod, have been exploited for cancer immunotherapy. Here, the authors design platelet membrane-cloaked nanoparticles for selective intratumoral delivery of resiquimod, resulting in potent anti-tumor immune response in a range of preclinical solid tumors.
Keywords	Science ; Q
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cardiac ischemia-reperfusion injury induces ROS-dependent loss of PKA regulatory subunit RIα.

Haushalter, Kristofer J / Schilling, Jan M / Song, Young / Sastri, Mira / Perkins, Guy A / Strack, Stefan / Taylor, Susan S / Patel, Hemal H

American journal of physiology. Heart and circulatory physiology

2019 Volume 317, Issue 6, Page(s) H1231–H1242

Abstract: Type I PKA regulatory α-subunit (RIα; encoded by the Prkar1a gene) serves as the predominant inhibitor protein of the catalytic subunit of cAMP-dependent protein kinase (PKAc). However, recent evidence suggests that PKA signaling can be initiated by cAMP- ...

Abstract	Type I PKA regulatory α-subunit (RIα; encoded by the Prkar1a gene) serves as the predominant inhibitor protein of the catalytic subunit of cAMP-dependent protein kinase (PKAc). However, recent evidence suggests that PKA signaling can be initiated by cAMP-independent events, especially within the context of cellular oxidative stress such as ischemia-reperfusion (I/R) injury. We determined whether RIα is actively involved in the regulation of PKA activity via reactive oxygen species (ROS)-dependent mechanisms during I/R stress in the heart. Induction of ex vivo global I/R injury in mouse hearts selectively downregulated RIα protein expression, whereas RII subunit expression appears to remain unaltered. Cardiac myocyte cell culture models were used to determine that oxidant stimulus (i.e., H
MeSH term(s)	A Kinase Anchor Proteins/genetics ; A Kinase Anchor Proteins/metabolism ; Animals ; Cell Line ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/genetics ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/ultrastructure ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Myocytes, Cardiac/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	A Kinase Anchor Proteins ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Reactive Oxygen Species
Language	English
Publishing date	2019-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00237.2019
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Article ; Online: Chronic β1-adrenoceptor blockade impairs ischaemic tolerance and preconditioning in murine myocardium.

See Hoe, Louise E / Schilling, Jan M / Busija, Anna R / Haushalter, Kristofer J / Ozberk, Victoria / Keshwani, Malik M / Roth, David M / Toit, Eugene Du / Headrick, John P / Patel, Hemal H / Peart, Jason N

European journal of pharmacology

2016 Volume 789, Page(s) 1–7

Abstract: β-adrenoceptor antagonists are commonly used in ischaemic heart disease (IHD) patients, yet may impair signalling and efficacy of 'cardioprotective' interventions. We assessed effects of chronic β1-adrenoceptor antagonism on myocardial resistance to ... ...

Abstract	β-adrenoceptor antagonists are commonly used in ischaemic heart disease (IHD) patients, yet may impair signalling and efficacy of 'cardioprotective' interventions. We assessed effects of chronic β1-adrenoceptor antagonism on myocardial resistance to ischaemia-reperfusion (IR) injury and the ability of cardioprotective interventions [classic ischaemic preconditioning (IPC); novel sustained ligand-activated preconditioning (SLP)] to reduce IR injury in murine hearts. Young male C57Bl/6 mice were untreated or received atenolol (0.5g/l in drinking water) for 4 weeks. Subsequently, two cardioprotective stimuli were evaluated: morphine pellets implanted (to induce SLP, controls received placebo) 5 days prior to Langendorff heart perfusion, and IPC in perfused hearts (3×1.5min ischaemia/2min reperfusion). Atenolol significantly reduced in vivo heart rate. Untreated control hearts exhibited substantial left ventricular dysfunction (~50% pressure development recovery, ~20mmHg diastolic pressure rise) with significant release of lactate dehydrogenase (LDH, tissue injury indicator) after 25min ischaemia/45min reperfusion. Contractile dysfunction and elevated LDH were reduced >50% with IPC and SLP. While atenolol treatment did not modify baseline contractile function, post-ischaemic function was significantly depressed compared to untreated hearts. Atenolol pre-treatment abolished beneficial effects of IPC, whereas SLP protection was preserved. These data indicate that chronic β1-adrenoceptor blockade can exert negative effects on functional IR tolerance and negate conventional IPC (implicating β1-adrenoceptors in IR injury and IPC signalling). However, novel morphine-induced SLP is resistant to inhibition by β1-adrenoceptor antagonism.
MeSH term(s)	Adrenergic beta-1 Receptor Antagonists/pharmacology ; Animals ; Dose-Response Relationship, Drug ; Heart Rate/drug effects ; Ischemic Preconditioning, Myocardial ; Isoproterenol/pharmacology ; L-Lactate Dehydrogenase/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Reperfusion Injury/enzymology ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/physiopathology ; Myocardial Reperfusion Injury/therapy ; Myocardium/metabolism ; Receptors, Adrenergic, beta-1/metabolism
Chemical Substances	Adrenergic beta-1 Receptor Antagonists ; Receptors, Adrenergic, beta-1 ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Isoproterenol (L628TT009W)
Language	English
Publishing date	2016-10-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2016.06.054
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Article ; Online: Hydrogen Sulfide--Mechanisms of Toxicity and Development of an Antidote.

Jiang, Jingjing / Chan, Adriano / Ali, Sameh / Saha, Arindam / Haushalter, Kristofer J / Lam, Wai-Ling Macrina / Glasheen, Megan / Parker, James / Brenner, Matthew / Mahon, Sari B / Patel, Hemal H / Ambasudhan, Rajesh / Lipton, Stuart A / Pilz, Renate B / Boss, Gerry R

Scientific reports

2016 Volume 6, Page(s) 20831

Abstract: Hydrogen sulfide is a highly toxic gas-second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known, and no specific therapy exists for sulfide poisoning. We show in several cell types, including ... ...

Abstract	Hydrogen sulfide is a highly toxic gas-second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known, and no specific therapy exists for sulfide poisoning. We show in several cell types, including human inducible pluripotent stem cell (hiPSC)-derived neurons, that sulfide inhibited complex IV of the mitochondrial respiratory chain and induced apoptosis. Sulfide increased hydroxyl radical production in isolated mouse heart mitochondria and F2-isoprostanes in brains and hearts of mice. The vitamin B12 analog cobinamide reversed the cellular toxicity of sulfide, and rescued Drosophila melanogaster and mice from lethal exposures of hydrogen sulfide gas. Cobinamide worked through two distinct mechanisms: direct reversal of complex IV inhibition and neutralization of sulfide-generated reactive oxygen species. We conclude that sulfide produces a high degree of oxidative stress in cells and tissues, and that cobinamide has promise as a first specific treatment for sulfide poisoning.
MeSH term(s)	Animals ; Antidotes/pharmacology ; Apoptosis ; Brain/drug effects ; Brain/metabolism ; Cell Differentiation ; Cobamides/pharmacology ; Drosophila melanogaster ; Electron Transport Complex IV/metabolism ; F2-Isoprostanes/antagonists & inhibitors ; F2-Isoprostanes/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Hydrogen Sulfide/antagonists & inhibitors ; Hydrogen Sulfide/toxicity ; Hydroxyl Radical/antagonists & inhibitors ; Hydroxyl Radical/metabolism ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/drug effects ; Induced Pluripotent Stem Cells/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/metabolism ; Myocardium/metabolism ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; Oxidative Stress ; Potassium Cyanide/antagonists & inhibitors ; Potassium Cyanide/toxicity ; Rats ; Sulfides/antagonists & inhibitors ; Sulfides/toxicity
Chemical Substances	Antidotes ; Cobamides ; F2-Isoprostanes ; Sulfides ; cobinamide (13497-85-3) ; Hydroxyl Radical (3352-57-6) ; Electron Transport Complex IV (EC 1.9.3.1) ; sodium bisulfide (FWU2KQ177W) ; Potassium Cyanide (MQD255M2ZO) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2016-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep20831
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Article ; Online: Nitrocobinamide, a new cyanide antidote that can be administered by intramuscular injection.

Chan, Adriano / Jiang, Jingjing / Fridman, Alla / Guo, Ling T / Shelton, G Diane / Liu, Ming-Tao / Green, Carol / Haushalter, Kristofer J / Patel, Hemal H / Lee, Jangwoen / Yoon, David / Burney, Tanya / Mukai, David / Mahon, Sari B / Brenner, Matthew / Pilz, Renate B / Boss, Gerry R

Journal of medicinal chemistry

2015 Volume 58, Issue 4, Page(s) 1750–1759

Abstract: Currently available cyanide antidotes must be given by intravenous injection over 5-10 min, making them ill-suited for treating many people in the field, as could occur in a major fire, an industrial accident, or a terrorist attack. These scenarios call ... ...

Abstract	Currently available cyanide antidotes must be given by intravenous injection over 5-10 min, making them ill-suited for treating many people in the field, as could occur in a major fire, an industrial accident, or a terrorist attack. These scenarios call for a drug that can be given quickly, e.g., by intramuscular injection. We have shown that aquohydroxocobinamide is a potent cyanide antidote in animal models of cyanide poisoning, but it is unstable in solution and poorly absorbed after intramuscular injection. Here we show that adding sodium nitrite to cobinamide yields a stable derivative (referred to as nitrocobinamide) that rescues cyanide-poisoned mice and rabbits when given by intramuscular injection. We also show that the efficacy of nitrocobinamide is markedly enhanced by coadministering sodium thiosulfate (reducing the total injected volume), and we calculate that ∼1.4 mL each of nitrocobinamide and sodium thiosulfate should rescue a human from a lethal cyanide exposure.
MeSH term(s)	Animals ; Antidotes/administration & dosage ; Antidotes/chemistry ; Antidotes/pharmacology ; COS Cells ; Cercopithecus aethiops ; Cobamides/administration & dosage ; Cobamides/chemistry ; Cobamides/pharmacology ; Cyanides/poisoning ; Dose-Response Relationship, Drug ; Injections, Intramuscular ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/drug effects ; Rabbits ; Sodium Nitrite/chemistry ; Structure-Activity Relationship ; Thiosulfates/administration & dosage ; Thiosulfates/chemistry ; Thiosulfates/pharmacology ; Time Factors
Chemical Substances	Antidotes ; Cobamides ; Cyanides ; Thiosulfates ; nitrocobinamide ; cobinamide (13497-85-3) ; sodium thiosulfate (HX1032V43M) ; Sodium Nitrite (M0KG633D4F)
Language	English
Publishing date	2015-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/jm501565k
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