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Book: Neural repair

Karamyan, Vardan T. / Stowe, Ann M.

methods and protocols

(Methods in molecular biology ; 2616 ; Springer protocols)

2023

Author's details	edited by Vardan T. Karamyan, Ann M. Stowe
Series title	Methods in molecular biology ; 2616 Springer protocols
Collection
Keywords	Nervous system/Diseases/Treatment ; Cerebrovascular disease/Treatment
Subject code	616.8043
Language	English
Size	xvi, 492 Seiten, Illustrationen, 26 cm
Publisher	Humana Press
Publishing place	New York, NY
Publishing country	United States
Document type	Book
HBZ-ID	HT021721759
ISBN	978-1-0716-2925-3 ; 9781071629260 ; 1-0716-2925-5 ; 1071629263
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Clinically Applicable Experimental Design and Considerations for Stroke Recovery Preclinical Studies.

Karamyan, Vardan T

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2616, Page(s) 369–377

Abstract: Development of stroke recovery therapies is an active field of research and represents an opportunity to reduce the global impact of stroke as the leading cause of acquired, long-term disability in adults. The negative outcomes of recent large-scale ... ...

Abstract	Development of stroke recovery therapies is an active field of research and represents an opportunity to reduce the global impact of stroke as the leading cause of acquired, long-term disability in adults. The negative outcomes of recent large-scale clinical trials have highlighted deficiencies in the translational process and endanger the trajectory of post-stroke recovery research. Because of this, a number of strategies have been recommended by experts to better navigate the translational pipeline. To assist the field in advancing to the next stage for successful clinical translation, the goal of this chapter is to discuss concepts relevant to the experimental design of in vivo preclinical pharmacological studies to make them clinically relevant and informative for future trials.
MeSH term(s)	Humans ; Stroke Rehabilitation ; Research Design ; Translational Research, Biomedical ; Stroke/drug therapy
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2926-0_25
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Article ; Online: Between two storms, vasoactive peptides or bradykinin underlie severity of COVID-19?

Karamyan, Vardan T

Physiological reports

2021 Volume 9, Issue 5, Page(s) e14796

Abstract: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to be a world-wide pandemic with overwhelming socioeconomic impact. Since inflammation is one of the major causes of COVID-19 ... ...

Abstract	Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to be a world-wide pandemic with overwhelming socioeconomic impact. Since inflammation is one of the major causes of COVID-19 complications, the associated molecular mechanisms have been the focus of many studies to better understand this disease and develop improved treatments for patients contracting SARS-CoV-2. Among these, strong emphasis has been placed on pro-inflammatory cytokines, associating severity of COVID-19 with so-called "cytokine storm." More recently, peptide bradykinin, its dysregulated signaling or "bradykinin storm," has emerged as a primary mechanism to explain COVID-19-related complications. Unfortunately, this important development may not fully capture the main molecular players that underlie the disease severity. To this end, in this focused review, several lines of evidence are provided to suggest that in addition to bradykinin, two closely related vasoactive peptides, substance P and neurotensin, are also likely to drive microvascular permeability and inflammation, and be responsible for development of COVID-19 pathology. Furthermore, based on published experimental observations, it is postulated that in addition to ACE and neprilysin, peptidase neurolysin (Nln) is also likely to contribute to accumulation of bradykinin, substance P and neurotensin, and progression of the disease. In conclusion, it is proposed that "vasoactive peptide storm" may underlie severity of COVID-19 and that simultaneous inhibition of all three peptidergic systems could be therapeutically more advantageous rather than modulation of any single mechanism alone.
MeSH term(s)	Animals ; Bradykinin/metabolism ; COVID-19/complications ; COVID-19/metabolism ; COVID-19/pathology ; Cytokines/metabolism ; Humans ; Microvessels/metabolism ; Microvessels/pathology ; Neprilysin/metabolism ; Neurotensin/metabolism ; Substance P/metabolism ; Post-Acute COVID-19 Syndrome
Chemical Substances	Cytokines ; Substance P (33507-63-0) ; Neurotensin (39379-15-2) ; Neprilysin (EC 3.4.24.11) ; Bradykinin (S8TIM42R2W)
Language	English
Publishing date	2021-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.14796
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A Low-Budget Photothrombotic Rodent Stroke Model.

Alamri, Faisal F / Karamyan, Serob T / Karamyan, Vardan T

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2616, Page(s) 21–28

Abstract: A number of animal stroke models have been developed and used over the years to study the pathological mechanisms of this disorder and develop new therapies. Among them, the photothrombotic model of ischemic stroke has been central in various studies ... ...

Abstract	A number of animal stroke models have been developed and used over the years to study the pathological mechanisms of this disorder and develop new therapies. Among them, the photothrombotic model of ischemic stroke has been central in various studies focusing on understanding of the basic biology of neural repair, identification and validation of key molecular targets involved in post-stroke recovery, and preclinical testing of various therapeutic approaches. To facilitate uniformity among various experimental groups using this expert-recommended mouse model of choice for stroke recovery studies, in this chapter we describe in detail a low-budget technique to induce photothrombosis in the mouse primary motor cortex. Additionally, we provide tips for conducting this procedure in other cerebral cortical regions of the mouse brain and in rats.
MeSH term(s)	Mice ; Rats ; Animals ; Rodentia ; Stroke/pathology ; Ischemic Stroke ; Disease Models, Animal ; Cerebral Cortex/pathology
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2926-0_3
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Article ; Online: Challenges with the proposed ACE2 activation mechanism of diminazene aceturate.

Esfahani, Shiva Hadi / Karamyan, Vardan T

Clinical and experimental pharmacology & physiology

2022 Volume 49, Issue 5, Page(s) 608–610

MeSH term(s)	Angiotensin-Converting Enzyme 2 ; Diminazene/analogs & derivatives ; Diminazene/pharmacology ; Renin-Angiotensin System
Chemical Substances	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; diminazene aceturate (JI8SAD85NO) ; Diminazene (Y5G36EEA5Z)
Language	English
Publishing date	2022-02-24
Publishing country	Australia
Document type	Letter ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	189277-0
ISSN	1440-1681 ; 0305-1870 ; 0143-9294
ISSN (online)	1440-1681
ISSN	0305-1870 ; 0143-9294
DOI	10.1111/1440-1681.13636
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Article: The role of peptidase neurolysin in neuroprotection and neural repair after stroke.

Karamyan, Vardan T

Neural regeneration research

2020 Volume 16, Issue 1, Page(s) 21–25

Abstract: Current experimental stroke research has evolved to focus on detailed understanding of the brain's self-protective and restorative mechanisms, and harness this knowledge for development of new therapies. In this context, the role of peptidases and ... ...

Abstract	Current experimental stroke research has evolved to focus on detailed understanding of the brain's self-protective and restorative mechanisms, and harness this knowledge for development of new therapies. In this context, the role of peptidases and neuropeptides is of growing interest. In this focused review, peptidase neurolysin (Nln) and its extracellular peptide substrates are briefly discussed in relation to pathophysiology of ischemic stroke. Upregulation of Nln following stroke is viewed as a compensatory cerebroprotective mechanism in the acute phase of stroke, because the main neuropeptides inactivated by Nln are neuro/cerebrotoxic (bradykinin, substance P, neurotensin, angiotensin II, hemopressin), whereas the peptides generated by Nln are neuro/cerebroprotective (angiotensin-(1-7), Leu-/Met-enkephalins). This notion is confirmed by experimental studies documenting aggravation of stroke outcomes in mice after inhibition of Nln following stroke, and dramatic improvement of stroke outcomes in mice overexpressing Nln in the brain. The role of Nln in the (sub)chronic phase of stroke is less clear and it is likely, that this peptidase does not have a major role in neural repair mechanisms. This is because, the substrates of Nln are less uniform in modulating neurorestorative mechanisms in one direction, some appearing to have neural repair enhancing/stimulating potential, whereas others doing the opposite. Future studies focusing on the role of Nln in pathophysiology of stroke should determine its potential as a cerebroprotective target for stroke therapy, because its unique ability to modulate multiple neuropeptide systems critically involved in brain injury mechanisms is likely advantageous over modulation of one pathogenic pathway for stroke pharmacotherapy.
Language	English
Publishing date	2020-08-13
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.284904
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Article ; Online: Peptidase neurolysin is an endogenous cerebroprotective mechanism in acute neurodegenerative disorders.

Karamyan, Vardan T

Medical hypotheses

2019 Volume 131, Page(s) 109309

Abstract: Stroke and traumatic brain injury (TBI) are significant clinical problems characterized by high rate of mortality and long-lasting disabilities, and an unmet need for new treatments. Current experimental stroke and TBI research are evolving to focus more ...

Abstract	Stroke and traumatic brain injury (TBI) are significant clinical problems characterized by high rate of mortality and long-lasting disabilities, and an unmet need for new treatments. Current experimental stroke and TBI research are evolving to focus more on understanding the brain's self-protective mechanisms to meet the critical need of developing new therapies for these disorders. In this hypothesis-based manuscript, I provide several lines of evidence that peptidase neurolysin (Nln) is one of the brain's potent, self-protective mechanisms promoting preservation and recovery of the brain after acute injury. Based on published experimental observations and ongoing studies in our laboratory, I posit that Nln is a compensatory and cerebroprotective mechanism in the post-stroke/TBI brain that functions to process a diverse group of extracellular neuropeptides and by that to reduce excitotoxicity, oxidative stress, edema formation, blood brain barrier hyper-permeability, and neuroinflammation. If this hypothesis is correct, Nln could potentially serve as a single therapeutic target to modulate the function of multiple targets, the involved neuropeptide systems, critically involved in various mechanisms of brain injury and cerebroprotection/restoration. Such multi-pathway target would be highly desired for pharmacotherapy of stroke and TBI, because targeting one pathophysiological pathway has proven to be ineffective for such complex disorders.
MeSH term(s)	Acute Disease ; Animals ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/physiopathology ; Cell Death ; Cell Hypoxia ; Cells, Cultured ; Cerebral Cortex/embryology ; Cerebral Cortex/metabolism ; Genetic Therapy ; Humans ; Metalloendopeptidases/biosynthesis ; Metalloendopeptidases/genetics ; Metalloendopeptidases/physiology ; Mice ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neuropeptides/metabolism ; Neurotoxins/pharmacology ; Olfactory Bulb/metabolism ; Oxidative Stress ; Oxygen/pharmacology ; Rats ; Recombinant Proteins/metabolism ; Renin-Angiotensin System/physiology ; Stroke/metabolism ; Stroke/physiopathology ; Stroke/therapy ; Up-Regulation
Chemical Substances	Nerve Tissue Proteins ; Neuropeptides ; Neurotoxins ; Recombinant Proteins ; Metalloendopeptidases (EC 3.4.24.-) ; neurolysin (EC 3.4.24.16) ; Oxygen (S88TT14065)
Language	English
Publishing date	2019-07-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	193145-3
ISSN	1532-2777 ; 0306-9877
ISSN (online)	1532-2777
ISSN	0306-9877
DOI	10.1016/j.mehy.2019.109309
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Article ; Online: Rodent Stroke Models to Study Functional Recovery and Neural Repair.

Britsch, Daimen R S / Syeara, Nausheen / Stowe, Ann M / Karamyan, Vardan T

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2616, Page(s) 3–12

Abstract: Rodent ischemic stroke models are essential research tools for studying this highly prevalent disease and represent a critical element in the translational pipeline for development of new therapies. The majority of ischemic stroke models have been ... ...

Abstract	Rodent ischemic stroke models are essential research tools for studying this highly prevalent disease and represent a critical element in the translational pipeline for development of new therapies. The majority of ischemic stroke models have been developed to study the acute phase of the disease and neuroprotective strategies, but a subset of models is better suited for studying stroke recovery. Each model therefore has characteristics that lend itself to certain types of investigations and outcome measures, and it is important to consider both explicit and implicit details when designing experiments that utilize each model. The following chapter briefly summarizes the known aspects of the main rodent stroke models with emphasis on their clinical relevance and suitability for studying recovery and neural repair following stroke.
MeSH term(s)	Animals ; Rodentia ; Stroke/therapy ; Ischemic Stroke ; Recovery of Function ; Disease Models, Animal
Language	English
Publishing date	2023-02-01
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2926-0_1
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Article ; Online: Small molecule neurolysin activators, potential multi-mechanism agents for ischemic stroke therapy.

Esfahani, Shiva Hadi / Abbruscato, Thomas J / Trippier, Paul C / Karamyan, Vardan T

Expert opinion on therapeutic targets

2022 Volume 26, Issue 5, Page(s) 401–404

MeSH term(s)	Brain/metabolism ; Humans ; Ischemic Stroke ; Metalloendopeptidases/metabolism ; Neuroprotective Agents ; Stroke/drug therapy
Chemical Substances	Neuroprotective Agents ; Metalloendopeptidases (EC 3.4.24.-) ; neurolysin (EC 3.4.24.16)
Language	English
Publishing date	2022-05-19
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2022.2077190
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Article ; Online: Is Diminazene an Angiotensin-Converting Enzyme 2 (ACE2) Activator? Experimental Evidence and Implications.

Esfahani, Shiva Hadi / Jayaraman, Srinidhi / Karamyan, Vardan T

The Journal of pharmacology and experimental therapeutics

2022 Volume 383, Issue 2, Page(s) 149–156

Abstract: Antiprotozoal veterinary drug diminazene aceturate (DIZE) has been proposed to be an angiotensin-converting enzyme 2 (ACE2) activator. Since then, DIZE was used in dozens of experimental studies, but its mechanism of action attributed to ACE2 activation ... ...

Abstract	Antiprotozoal veterinary drug diminazene aceturate (DIZE) has been proposed to be an angiotensin-converting enzyme 2 (ACE2) activator. Since then, DIZE was used in dozens of experimental studies, but its mechanism of action attributed to ACE2 activation and enhanced formation of angiontensin-(1-7) [Ang-(1-7)] from Ang II was not carefully verified. The aim of this study was to confirm the effect of DIZE on catalytic activity of ACE2 and extend it to other peptidases involved in formation and degradation of Ang-(1-7). Concentration-dependent effect of DIZE on the initial rate of a fluorogenic substrate hydrolysis by human and mouse recombinant ACE2 was measured at assay conditions imitating that of the original report, but no activation of ACE2 was documented. Similar results were obtained with a more physiologically relevant assay buffer. In addition, DIZE did not affect activity of recombinant neprilysin, neurolysin, thimet oligopeptidase, and ACE. Efficiency of the fluorogenic substrate hydrolysis (V
MeSH term(s)	Mice ; Humans ; Animals ; Angiotensin-Converting Enzyme 2 ; Fluorescent Dyes ; Peptidyl-Dipeptidase A/metabolism ; Peptide Fragments/pharmacology
Chemical Substances	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Fluorescent Dyes ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Peptide Fragments
Language	English
Publishing date	2022-09-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.122.001339
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