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Article: New protocol for kinetic assay seeding ability recovery "KASAR" from formalin-fixed paraffin-embedded tissues.

Hepker, Monica / Clabaugh, Griffin / Jin, Huajun / Kanthasamy, Anumantha G

2023 Volume 10, Page(s) 1087982

Abstract: The real-time quaking-induced conversion (RT-QuIC) alpha-synuclein (aSyn) protein kinetic seeding assay has been very useful for detecting pathological aggregates in various synucleinopathies including Parkinson's disease (PD). This biomarker assay ... ...

Abstract	The real-time quaking-induced conversion (RT-QuIC) alpha-synuclein (aSyn) protein kinetic seeding assay has been very useful for detecting pathological aggregates in various synucleinopathies including Parkinson's disease (PD). This biomarker assay relies on fresh frozen tissue to effectively seed and amplify aSyn aggregating protein. With vast repositories of formalin-fixed paraffin-embedded (FFPE) tissues, it is paramount to harness the power of kinetic assays to unlock the diagnostic potential of archived FFPE biospecimens. However, the major challenge posed by significantly reduced amplification of formalin-fixed tissues in the assay suggests that formalin fixation deterred monomer interaction with the sample seed and depressed subsequent protein aggregation. To overcome this challenge, we developed a kinetic assay seeding ability recovery (KASAR) protocol to maintain the integrity of the tissue and seeding protein. For this, we implemented a series of heating steps with the brain tissue suspended in a buffer composed of 500 mM tris-HCl (pH 7.5) and 0.02% SDS after the standard deparaffinization of the tissue sections. Initially, samples from seven human brain samples, including four samples from patients diagnosed with dementia with Lewy bodies (DLB) and three samples from healthy controls without DLB, were compared to fresh frozen samples under three different, but clinically common sample storage conditions: formalin-fixed, FFPE, and FFPE slices cut 5 µm thick. The KASAR protocol was able to recover seeding activity for all positive samples in all storage conditions. Next, 28 FFPE samples from the submandibular gland (SMG) of patients diagnosed with PD, incidental Lewy body disease (ILBD), or healthy controls were tested with 93% of results replicating when blinded. With samples of only a few milligrams, this protocol recovered the same quality of seeding in formalin-fixed tissue as fresh frozen tissue. Moving forward, protein aggregate kinetic assays, in conjunction with the KASAR protocol, can be used to understand and diagnose neurodegenerative diseases more comprehensively. Overall, our KASAR protocol unlocks and restores the seeding ability of formalin-fixed paraffin-embedded tissues for the amplification of biomarker protein aggregates in kinetic assays.
Language	English
Publishing date	2023-01-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2023.1087982
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Article ; Online: Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation.

Huang, Minhong / Malovic, Emir / Ealy, Alyssa / Jin, Huajun / Anantharam, Vellareddy / Kanthasamy, Arthi / Kanthasamy, Anumantha G

Frontiers in immunology

2023 Volume 14, Page(s) 1052925

Abstract: Epigenetic reprogramming is the ability of innate immune cells to form memories of environmental stimuli (priming), allowing for heightened responses to secondary stressors. Herein, we explored microglial epigenetic marks using the known inflammagen LPS ... ...

Abstract	Epigenetic reprogramming is the ability of innate immune cells to form memories of environmental stimuli (priming), allowing for heightened responses to secondary stressors. Herein, we explored microglial epigenetic marks using the known inflammagen LPS as a memory priming trigger and Parkinsonian-linked environmental neurotoxic stressor manganese (Mn) as the secondary environmental trigger. To mimic physiological responses, the memory priming trigger LPS treatment was removed by triple-washing to allow the cells' acute inflammatory response to reset back before applying the secondary insult. Our results show that after the secondary Mn insult, levels of key proinflammatory markers, including nitrite release, iNOS mRNA and protein expression, Il-6, Il-α and cytokines were exaggerated in LPS-primed microglia. Our paradigm implies primed microglia retain immune memory that can be reprogrammed to augment inflammatory response by secondary environmental stress. To ascertain the molecular underpinning of this neuroimmune memory, we further hypothesize that epigenetic reprogramming contributes to the retention of a heightened immune response. Interestingly, Mn-exposed, LPS-primed microglia showed enhanced deposition of H3K27ac and H3K4me3 along with H3K4me1. We further confirmed the results using a PD mouse model (MitoPark) and postmortem human PD brains, thereby adding clinical relevance to our findings. Co-treatment with the p300/H3K27ac inhibitor GNE-049 reduced p300 expression and H3K27ac deposition, decreased iNOS, and increased ARG1 and IRF4 levels. Lastly, since mitochondrial stress is a driver of environmentally linked Parkinson's disease (PD) progression, we examined the effects of GNE-049 on primary trigger-induced mitochondrial stress. GNE-049 reduced mitochondrial superoxide, mitochondrial circularity and stress, and mitochondrial membrane depolarization, suggesting beneficial consequences of GNE-049 on mitochondrial function. Collectively, our findings demonstrate that proinflammatory primary triggers can shape microglial memory
MeSH term(s)	Mice ; Animals ; Humans ; Neuroinflammatory Diseases ; Microglia ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; Acetylation ; Histones/metabolism ; Parkinson Disease/metabolism ; Epigenesis, Genetic
Chemical Substances	Lipopolysaccharides ; Histones
Language	English
Publishing date	2023-03-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1052925
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Article: Construction of surface molecularly imprinted photonic hydrogel sensors with high sensitivity

Yang, Zhaokun / Jin, Huajun / Yu, Ang / Yu, Zhangyong / Shi, Dongjian / Yan, Shengrong / Qin, Liyan / Liu, Shirong / Chen, Mingqing

Colloids and surfaces. 2022 Apr. 20, v. 639

2022

Abstract: In comparison with molecularly imprinted photonic hydrogel (MIPH) with specific molecular recognition sites inside matrix, surface molecularly imprinted photonic hydrogel (S-MIPH) is more competitive as a molecular sensor due to presence of molecular ... ...

Abstract	In comparison with molecularly imprinted photonic hydrogel (MIPH) with specific molecular recognition sites inside matrix, surface molecularly imprinted photonic hydrogel (S-MIPH) is more competitive as a molecular sensor due to presence of molecular recognition sites distributed on surface of hydrogel wall. Nevertheless, the construction of S-MIPH sensors is still challenging owing to the absence of interaction between traditional colloids and imprinted molecules. Here we report the construction of S-MIPH sensors by using poly (styrene-acrylic acid) colloids with abundant carboxyl group that are capable of binding imprinted molecules readily through hydrogen interaction. Benefit from this novel motif, S-MIPH sensors can be readily constructed by self-assembly of poly (styrene-acrylic acid) colloids binding imprinted molecules, the polymerization of precursor solution, as well as finally removal of colloids and imprinted molecules. The self-assembly of poly (styrene-acrylic acid) colloids binding imprinted molecules was investigated in detail. The as-prepared sensor delivers high sensitivity (as low as 10⁻⁹ mol L⁻¹), rapid response speed (< 60 s), and good selectivity owing to the 3D macroporous structure and specific molecular recognition sites that are well distributed on surface of hydrogel wall. Additionally, the developed sensors show good sensing performance even in commercial milk, showing great potential for real application.
Keywords	hydrogels ; hydrogen ; milk ; photons ; polymerization ; porous media
Language	English
Dates of publication	2022-0420
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	1500517-3
ISSN	0927-7757
ISSN	0927-7757
DOI	10.1016/j.colsurfa.2022.128341
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Article: Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson's disease.

Ay, Muhammet / Charli, Adhithiya / Langley, Monica / Jang, Ahyoung / Padhi, Piyush / Jin, Huajun / Anantharam, Vellareddy / Kalyanaraman, Balaraman / Kanthasamy, Arthi / Kanthasamy, Anumantha G

Frontiers in neuroscience

2024 Volume 18, Page(s) 1356703

Abstract: Impaired mitochondrial function and biogenesis have strongly been implicated in the pathogenesis of Parkinson's disease (PD). Thus, identifying the key signaling mechanisms regulating mitochondrial biogenesis is crucial to developing new treatment ... ...

Abstract	Impaired mitochondrial function and biogenesis have strongly been implicated in the pathogenesis of Parkinson's disease (PD). Thus, identifying the key signaling mechanisms regulating mitochondrial biogenesis is crucial to developing new treatment strategies for PD. We previously reported that protein kinase D1 (PKD1) activation protects against neuronal cell death in PD models by regulating mitochondrial biogenesis. To further harness the translational drug discovery potential of targeting PKD1-mediated neuroprotective signaling, we synthesized mito-metformin (Mito-Met), a mitochondria-targeted analog derived from conjugating the anti-diabetic drug metformin with a triphenylphosphonium functional group, and then evaluated the preclinical efficacy of Mito-Met in cell culture and MitoPark animal models of PD. Mito-Met (100-300 nM) significantly activated PKD1 phosphorylation, as well as downstream Akt and AMPKα phosphorylation, more potently than metformin, in N27 dopaminergic neuronal cells. Furthermore, treatment with Mito-Met upregulated the mRNA and protein expression of mitochondrial transcription factor A (TFAM) implying that Mito-Met can promote mitochondrial biogenesis. Interestingly, Mito-Met significantly increased mitochondrial bioenergetics capacity in N27 dopaminergic cells. Mito-Met also reduced mitochondrial fragmentation induced by the Parkinsonian neurotoxicant MPP
Language	English
Publishing date	2024-02-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2024.1356703
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Article ; Online: Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson's Disease.

Huang, Minhong / Bargues-Carot, Alejandra / Riaz, Zainab / Wickham, Hannah / Zenitsky, Gary / Jin, Huajun / Anantharam, Vellareddy / Kanthasamy, Arthi / Kanthasamy, Anumantha G

International journal of molecular sciences

2022 Volume 23, Issue 18

Abstract: As a prevalent progressive neurodegenerative disorder, Parkinson's disease (PD) is characterized by the neuropathological hallmark of the loss of nigrostriatal dopaminergic (DAergic) innervation and the appearance of Lewy bodies with aggregated α- ... ...

Abstract	As a prevalent progressive neurodegenerative disorder, Parkinson's disease (PD) is characterized by the neuropathological hallmark of the loss of nigrostriatal dopaminergic (DAergic) innervation and the appearance of Lewy bodies with aggregated α-synuclein. Although several familial forms of PD have been reported to be associated with several gene variants, most cases in nature are sporadic, triggered by a complex interplay of genetic and environmental risk factors. Numerous epidemiological studies during the past two decades have shown positive associations between PD and several environmental factors, including exposure to neurotoxic pesticides/herbicides and heavy metals as well as traumatic brain injury. Other environmental factors that have been implicated as potential risk factors for PD include industrial chemicals, wood pulp mills, farming, well-water consumption, and rural residence. In this review, we summarize the environmental toxicology of PD with the focus on the elaboration of chemical toxicity and the underlying pathogenic mechanisms associated with exposure to several neurotoxic chemicals, specifically 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, paraquat (PQ), dichloro-diphenyl-trichloroethane (DDT), dieldrin, manganese (Mn), and vanadium (V). Our overview of the current findings from cellular, animal, and human studies of PD provides information for possible intervention strategies aimed at halting the initiation and exacerbation of environmentally linked PD.
MeSH term(s)	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Animals ; DDT ; Dieldrin/metabolism ; Herbicides/metabolism ; Humans ; Manganese/metabolism ; Mitochondria/metabolism ; Neuroinflammatory Diseases ; Neurotoxicity Syndromes/pathology ; Oxidative Stress ; Paraquat ; Parkinson Disease/metabolism ; Pesticides/metabolism ; Pesticides/toxicity ; Risk Factors ; Rotenone/metabolism ; Trichloroethanes/metabolism ; Vanadium/metabolism ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism
Chemical Substances	Herbicides ; Pesticides ; Trichloroethanes ; alpha-Synuclein ; Vanadium (00J9J9XKDE) ; Rotenone (03L9OT429T) ; Manganese (42Z2K6ZL8P) ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (9P21XSP91P) ; DDT (CIW5S16655) ; Dieldrin (I0246D2ZS0) ; Paraquat (PLG39H7695)
Language	English
Publishing date	2022-09-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231810808
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Article: Mechanistic Insights Into Gut Microbiome Dysbiosis-Mediated Neuroimmune Dysregulation and Protein Misfolding and Clearance in the Pathogenesis of Chronic Neurodegenerative Disorders.

Padhi, Piyush / Worth, Carter / Zenitsky, Gary / Jin, Huajun / Sambamurti, Kumar / Anantharam, Vellareddy / Kanthasamy, Arthi / Kanthasamy, Anumantha G

Frontiers in neuroscience

2022 Volume 16, Page(s) 836605

Abstract: The human gut microbiota is a complex, dynamic, and highly diverse community of microorganisms. Beginning as early ... ...

Abstract	The human gut microbiota is a complex, dynamic, and highly diverse community of microorganisms. Beginning as early as
Language	English
Publishing date	2022-02-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.836605
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Article: Environmental neurotoxic pesticide exposure induces gut inflammation and enteric neuronal degeneration by impairing enteric glial mitochondrial function in pesticide models of Parkinson’s disease: Potential relevance to gut-brain axis inflammation in Parkinson’s disease pathogenesis

Palanisamy, Bharathi N. / Sarkar, Souvarish / Malovic, Emir / Samidurai, Manikandan / Charli, Adhithiya / Zenitsky, Gary / Jin, Huajun / Anantharam, Vellareddy / Kanthasamy, Arthi / Kanthasamy, Anumantha G.

international journal of biochemistry & cell biology. 2022 June, v. 147

2022

Abstract: Despite the growing recognition that gastrointestinal (GI) dysfunction is prevalent in Parkinson's disease (PD) and occurs as a major prodromal symptom of PD, its cellular and molecular mechanisms remain largely unknown. Among the various types of GI ... ...

Abstract	Despite the growing recognition that gastrointestinal (GI) dysfunction is prevalent in Parkinson's disease (PD) and occurs as a major prodromal symptom of PD, its cellular and molecular mechanisms remain largely unknown. Among the various types of GI cells, enteric glial cells (EGCs), which resemble astrocytes in structure and function, play a critical role in the pathophysiology of many GI diseases including PD. Thus, we investigated how EGCs respond to the environmental pesticides rotenone (Rot) and tebufenpyrad (Tebu) in cell and animal models to better understand the mechanism underlying GI abnormalities. Both Rot and Tebu induce dopaminergic neuronal cell death through complex 1 inhibition of the mitochondrial respiratory chain. We report that exposing a rat enteric glial cell model (CRL-2690 cells) to these pesticides increased mitochondrial fission and reduced mitochondrial fusion by impairing MFN2 function. Furthermore, they also increased mitochondrial superoxide generation and impaired mitochondrial ATP levels and basal respiratory rate. Measurement of LC3, p62 and lysosomal assays revealed impaired autolysosomal function in ECGs during mitochondrial stress. Consistent with our recent findings that mitochondrial dysfunction augments inflammation in astrocytes and microglia, we found that neurotoxic pesticide exposure also enhanced the production of pro-inflammatory factors in EGCs in direct correlation with the loss in mitochondrial mass. Finally, we show that pesticide-induced mitochondrial defects functionally impaired smooth muscle velocity, acceleration, and total kinetic energy in a mixed primary culture of the enteric nervous system (ENS). Collectively, our studies demonstrate for the first time that exposure to environmental neurotoxic pesticides impairs mitochondrial bioenergetics and activates inflammatory pathways in EGCs, further augmenting mitochondrial dysfunction and pro-inflammatory events to induce gut dysfunction. Our findings have major implications in understanding the GI-related pathogenesis and progression of environmentally linked PD.
Keywords	Parkinson disease ; astrocytes ; cell death ; electron transport chain ; gastrointestinal system ; inflammation ; kinetic energy ; mitochondria ; neurons ; neurotoxicity ; pathogenesis ; pathophysiology ; pesticides ; rats ; respiratory rate ; rotenone ; smooth muscle
Language	English
Dates of publication	2022-06
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2022.106225
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Article: Epitranscriptomic Reader YTHDF2 Regulates SEK1(

Malovic, Emir / Ealy, Alyssa / Hsu, Phillip J / Sarkar, Souvarish / Miller, Cameron / Rokad, Dharmin / Goeser, Cody / Hartman, Aleah Kristen / Zhu, Allen / Palanisamy, Bharathi / Zenitsky, Gary / Jin, Huajun / Anantharam, Vellareddy / Kanthasamy, Arthi / He, Chuan / Kanthasamy, Anumantha G

bioRxiv : the preprint server for biology

2024

Abstract: As the most abundant glial cells in the CNS, astrocytes dynamically respond to neurotoxic stress, however, the key molecular regulators controlling the inflammatory status of these sentinels during neurotoxic stress have remained elusive. Herein, we ... ...

Abstract	As the most abundant glial cells in the CNS, astrocytes dynamically respond to neurotoxic stress, however, the key molecular regulators controlling the inflammatory status of these sentinels during neurotoxic stress have remained elusive. Herein, we demonstrate that the m6A epitranscriptomic mRNA modification tightly regulates the pro-inflammatory functions of astrocytes. Specifically, the astrocytic neurotoxic stresser, manganese (Mn), downregulated the m6A reader YTHDF2 in human and mouse astrocyte cultures and in the mouse brain. Functionally, YTHDF2 knockdown augmented, while its overexpression dampened, neurotoxic stress induced proinflammatory response, suggesting YTHDF2 serves as a key upstream regulator of inflammatory responses in astrocytes. Mechnistically, YTHDF2 RIP-sequencing identified
Language	English
Publishing date	2024-01-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.26.577106
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Article ; Online: Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms.

Kanthasamy, Arthi / Jin, Huajun / Charli, Adhithiya / Vellareddy, Anantharam / Kanthasamy, Anumantha

Pharmacology & therapeutics

2019 Volume 197, Page(s) 61–82

Abstract: With the increased incidence of neurodegenerative diseases worldwide, Parkinson's disease (PD) represents the second-most common neurodegenerative disease. PD is a progressive multisystem neurodegenerative disorder characterized by a marked loss of ... ...

Abstract	With the increased incidence of neurodegenerative diseases worldwide, Parkinson's disease (PD) represents the second-most common neurodegenerative disease. PD is a progressive multisystem neurodegenerative disorder characterized by a marked loss of nigrostriatal dopaminergic neurons and the formation of Lewy pathology in diverse brain regions. Although the mechanisms underlying dopaminergic neurodegeneration remain poorly characterized, data from animal models and postmortem studies have revealed that heightened inflammatory responses mediated via microglial and astroglial activation and the resultant release of proinflammatory factors may act as silent drivers of neurodegeneration. In recent years, numerous studies have demonstrated a positive association between the exposure to environmental neurotoxicants and the etiology of PD. Although it is unclear whether neuroinflammation drives pesticide-induced neurodegeneration, emerging evidence suggests that the failure to dampen neuroinflammatory mechanisms may account for the increased vulnerability to pesticide neurotoxicity. Furthermore, recent studies provide additional evidence that shifts the focus from a neuron-centric view to glial-associated neurodegeneration following pesticide exposure. In this review, we propose to summarize briefly the possible factors that regulate neuroinflammatory processes during environmental neurotoxicant exposure with a focus on the potential roles of mitochondria-driven redox mechanisms. In this context, a critical discussion of the data obtained from experimental research and possible epidemiological studies is included. Finally, we hope to provide insights on the pivotal role of exosome-mediated intercellular transmission of aggregated proteins in microglial activation response and the resultant dopaminergic neurodegeneration after exposure to pesticides. Collectively, an improved understanding of glia-mediated neuroinflammatory signaling might provide novel insights into the mechanisms that contribute to neurodegeneration induced by environmental neurotoxicant exposure.
MeSH term(s)	Animals ; Dopaminergic Neurons/pathology ; Exosomes ; Humans ; Neurodegenerative Diseases/pathology ; Neurotoxicity Syndromes/pathology ; Oxidative Stress
Language	English
Publishing date	2019-01-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2019.01.001
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Article: Cancer vaccine: learning lessons from immune checkpoint inhibitors.

Ye, ZhenLong / Qian, Qiming / Jin, HuaJun / Qian, QiJun

Journal of Cancer

2018 Volume 9, Issue 2, Page(s) 263–268

Abstract: Cancer vaccines have been exclusively studied all through the past decades, and have made exceptional achievements in cancer treatment. Few cancer vaccines have been approved by the US Food and Drug Administration (FDA), for instance, Provenge, which was ...

Abstract	Cancer vaccines have been exclusively studied all through the past decades, and have made exceptional achievements in cancer treatment. Few cancer vaccines have been approved by the US Food and Drug Administration (FDA), for instance, Provenge, which was approved for the treatment of prostate carcinoma in 2012. Moreover, more recently, T-VEC got approval for the treatment of melanoma. While, the overall therapeutic effects of cancer vaccines have been taken into consideration as below expectations, low antigenicity of targeting antigen and tumor heterogeneity are the two key limiting barriers encountered by the cancer vaccines. Nonetheless, recent developments in cancer immune-therapies together with associated technologies, for instance the unparalleled achievements bagged by immune checkpoint inhibitor based therapies and neo-antigen identification tools, envisage potential improvements in cancer vaccines in respect to the treatments of malignancies. This review brings forth measures for the purpose of refining therapeutic cancer vaccines by learning lessons from the success of PD-1 inhibitor based immune-therapies.
Language	English
Publishing date	2018-01-01
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.20059
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