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Article: Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis.

Abbasi, Mojdeh / Gupta, Vivek / Chitranshi, Nitin / Moustardas, Petros / Ranjbaran, Reza / Graham, Stuart L

2023

Abstract: Glaucoma is a common retinal disorder characterized by progressive optic nerve damage, resulting in visual impairment and potential blindness. Elevated intraocular pressure (IOP) is a major risk factor, but some patients still experience disease ... ...

Abstract	Glaucoma is a common retinal disorder characterized by progressive optic nerve damage, resulting in visual impairment and potential blindness. Elevated intraocular pressure (IOP) is a major risk factor, but some patients still experience disease progression despite IOP-lowering treatments. Genome-wide association studies have linked variations in the Caveolin1/2 (CAV-1/2) gene loci to glaucoma risk. Cav-1, a key protein in caveolae membrane invaginations, is involved in signaling pathways and its absence impairs retinal function. Recent research suggests that Cav-1 is implicated in modulating the BDNF/TrkB signaling pathway in retinal ganglion cells, which plays a critical role in retinal ganglion cell (RGC) health and protection against apoptosis. Understanding the interplay between these proteins could shed light on glaucoma pathogenesis and provide potential therapeutic targets.
Language	English
Publishing date	2023-11-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2625789-0
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2023.1012
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Article ; Online: Glial Cell Activation and Immune Responses in Glaucoma: A Systematic Review of Human Postmortem Studies of the Retina and Optic Nerve.

Salkar, Akanksha / Wall, Roshana Vander / Basavarajappa, Devaraj / Chitranshi, Nitin / Parilla, Gabriella E / Mirzaei, Mehdi / Yan, Peng / Graham, Stuart / You, Yuyi

Aging and disease

2024

Abstract: Although researched extensively the understanding regarding mechanisms underlying glaucoma pathogenesis remains limited. Further, the exact mechanism behind neuronal death remains elusive. The role of neuroinflammation in retinal ganglion cell (RGC) ... ...

Abstract	Although researched extensively the understanding regarding mechanisms underlying glaucoma pathogenesis remains limited. Further, the exact mechanism behind neuronal death remains elusive. The role of neuroinflammation in retinal ganglion cell (RGC) death has been prominently theorised. This review provides a comprehensive summary of neuroinflammatory responses in glaucoma. A systematic search of Medline and Embase for articles published up to 8th March 2023 yielded 32 studies using post-mortem tissues from glaucoma patients. The raw data were extracted from tables and text to calculate the standardized mean differences (SMDs). These studies utilized post-mortem tissues from glaucoma patients, totalling 490 samples, compared with 380 control samples. Among the included studies, 27 reported glial cell activation based on changes to cellular morphology and molecular staining. Molecular changes were predominantly attributed to astrocytes (62.5%) and microglia (15.6%), with some involvement of Muller cells. These glial cell changes included amoeboid microglial cells with increased CD45 or HLA-DR intensity and hypertrophied astrocytes with increased glial fibrillary acidic protein labelling. Further, changes to extracellular matrix proteins like collagen, galectin, and tenascin-C suggested glial cells' influence on structural changes in the optic nerve head. The activation of DAMPs-driven immune response and the classical complement cascade was reported and found to be associated with activated glial cells in glaucomatous tissue. Increased pro-inflammatory markers such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were also linked to glial cells. Glial cell activation was also associated with mitochondrial, vascular, metabolic and antioxidant component disruptions. Association of the activated glial cells with pro-inflammatory responses, dysregulation of homeostatic components and antigen presentation indicates that glial cell responses influence glaucoma progression. However, the exact mechanism triggering these responses and underlying interactions remains unexplored. This necessitates further research using human samples for an increased understanding of the precise role of neuroinflammation in glaucoma progression.
Language	English
Publishing date	2024-03-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2625789-0
ISSN	2152-5250 ; 2152-5250
ISSN (online)	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2024.0103
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Article ; Online: Extracellular vesicles as reconfigurable therapeutics for eye diseases: Promises and hurdles.

Shekari, Faezeh / Abyadeh, Morteza / Meyfour, Anna / Mirzaei, Mehdi / Chitranshi, Nitin / Gupta, Vivek / Graham, Stuart L / Salekdeh, Ghasem Hosseini

Progress in neurobiology

2023 Volume 225, Page(s) 102437

Abstract: A large number of people worldwide suffer from visual impairment. However, most available therapies rely on impeding the development of a particular eye disorder. Therefore, there is an increasing demand for effective alternative treatments, specifically ...

Abstract	A large number of people worldwide suffer from visual impairment. However, most available therapies rely on impeding the development of a particular eye disorder. Therefore, there is an increasing demand for effective alternative treatments, specifically regenerative therapies. Extracellular vesicles, including exosomes, ectosomes, or microvesicles, are released by cells and play a potential role in regeneration. Following an introduction to EV biogenesis and isolation methods, this integrative review provides an overview of our current knowledge about EVs as a communication paradigm in the eye. Then, we focused on the therapeutic applications of EVs derived from conditioned medium, biological fluid, or tissue and highlighted some recent developments in strategies to boost the innate therapeutic potential of EVs by loading various kinds of drugs or being engineered at the level of producing cells or EVs. Challenges faced in the development of safe and effective translation of EV-based therapy into clinical settings for eye diseases are also discussed to pave the road toward reaching feasible regenerative therapies required for eye-related complications.
MeSH term(s)	Humans ; Extracellular Vesicles ; Exosomes
Language	English
Publishing date	2023-03-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2023.102437
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Article: Quantitative Proteomics Reveal Region-Specific Alterations in Neuroserpin-Deficient Mouse Brain and Retina: Insights into Serpini1 Function.

Mirshahvaladi, Shahab / Chitranshi, Nitin / Amirkhani, Ardeshir / Rajput, Rashi / Basavarajappa, Devaraj / Vander Wall, Roshana / Pascovici, Dana / Godinez, Angela / Galliciotti, Giovanna / Paulo, Joao A / Gupta, Veer / Graham, Stuart L / Gupta, Vivek / Mirzaei, Mehdi

Proteomes

2024 Volume 12, Issue 1

Abstract: Neural regeneration and neuroprotection represent strategies for future management of neurodegenerative disorders such as Alzheimer's disease (AD) or glaucoma. However, the complex molecular mechanisms that are involved in neuroprotection are not clearly ...

Abstract	Neural regeneration and neuroprotection represent strategies for future management of neurodegenerative disorders such as Alzheimer's disease (AD) or glaucoma. However, the complex molecular mechanisms that are involved in neuroprotection are not clearly understood. A promising candidate that maintains neuroprotective signaling networks is neuroserpin (Serpini1), a serine protease inhibitor expressed in neurons which selectively inhibits extracellular tissue-type plasminogen activator (tPA)/plasmin and plays a neuroprotective role during ischemic brain injury. Abnormal function of this protein has been implicated in several conditions including stroke, glaucoma, AD, and familial encephalopathy with neuroserpin inclusion bodies (FENIB). Here, we explore the potential biochemical roles of Serpini1 by comparing proteome changes between neuroserpin-deficient (NS
Language	English
Publishing date	2024-03-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720995-7
ISSN	2227-7382
ISSN	2227-7382
DOI	10.3390/proteomes12010007
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Article ; Online: Signalling pathways and cell death mechanisms in glaucoma: Insights into the molecular pathophysiology.

Basavarajappa, Devaraj / Galindo-Romero, Caridad / Gupta, Vivek / Agudo-Barriuso, Marta / Gupta, Veer B / Graham, Stuart L / Chitranshi, Nitin

Molecular aspects of medicine

2023 Volume 94, Page(s) 101216

Abstract: Glaucoma is a complex multifactorial eye disease manifesting in retinal ganglion cell (RGC) death and optic nerve degeneration, ultimately causing irreversible vision loss. Research in recent years has significantly enhanced our understanding of RGC ... ...

Abstract	Glaucoma is a complex multifactorial eye disease manifesting in retinal ganglion cell (RGC) death and optic nerve degeneration, ultimately causing irreversible vision loss. Research in recent years has significantly enhanced our understanding of RGC degenerative mechanisms in glaucoma. It is evident that high intraocular pressure (IOP) is not the only contributing factor to glaucoma pathogenesis. The equilibrium of pro-survival and pro-death signalling pathways in the retina strongly influences the function and survival of RGCs and optic nerve axons in glaucoma. Molecular evidence from human retinal tissue analysis and a range of experimental models of glaucoma have significantly contributed to unravelling these mechanisms. Accumulating evidence reveals a wide range of molecular signalling pathways that can operate -either alone or via intricate networks - to induce neurodegeneration. The roles of several molecules, including neurotrophins, interplay of intracellular kinases and phosphates, caveolae and adapter proteins, serine proteases and their inhibitors, nuclear receptors, amyloid beta and tau, and how their dysfunction affects retinal neurons are discussed in this review. We further underscore how anatomical alterations in various animal models exhibiting RGC degeneration and susceptibility to glaucoma-related neuronal damage have helped to characterise molecular mechanisms in glaucoma. In addition, we also present different regulated cell death pathways that play a critical role in RGC degeneration in glaucoma.
MeSH term(s)	Animals ; Humans ; Amyloid beta-Peptides/metabolism ; Glaucoma/genetics ; Glaucoma/metabolism ; Glaucoma/pathology ; Retina/metabolism ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology ; Cell Death ; Disease Models, Animal
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-10-17
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2023.101216
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Article ; Online: The role of myelin in neurodegeneration: implications for drug targets and neuroprotection strategies.

Parrilla, Gabriella E / Gupta, Vivek / Wall, Roshana Vander / Salkar, Akanksha / Basavarajappa, Devaraj / Mirzaei, Mehdi / Chitranshi, Nitin / Graham, Stuart L / You, Yuyi

Reviews in the neurosciences

2023 Volume 35, Issue 3, Page(s) 271–292

Abstract: Myelination of axons in the central nervous system offers numerous advantages, including decreased energy expenditure for signal transmission and enhanced signal speed. The myelin sheaths surrounding an axon consist of a multi-layered membrane that is ... ...

Abstract	Myelination of axons in the central nervous system offers numerous advantages, including decreased energy expenditure for signal transmission and enhanced signal speed. The myelin sheaths surrounding an axon consist of a multi-layered membrane that is formed by oligodendrocytes, while specific glycoproteins and lipids play various roles in this formation process. As beneficial as myelin can be, its dysregulation and degeneration can prove detrimental. Inflammation, oxidative stress, and changes in cellular metabolism and the extracellular matrix can lead to demyelination of these axons. These factors are hallmark characteristics of certain demyelinating diseases including multiple sclerosis. The effects of demyelination are also implicated in primary degeneration in diseases such as glaucoma and Alzheimer's disease, as well as in processes of secondary degeneration. This reveals a relationship between myelin and secondary processes of neurodegeneration, including resultant degeneration following traumatic injury and transsynaptic degeneration. The role of myelin in primary and secondary degeneration is also of interest in the exploration of strategies and targets for remyelination, including the use of anti-inflammatory molecules or nanoparticles to deliver drugs. Although the use of these methods in animal models of diseases have shown to be effective in promoting remyelination, very few clinical trials in patients have met primary end points. This may be due to shortcomings or considerations that are not met while designing a clinical trial that targets remyelination. Potential solutions include diversifying disease targets and requiring concomitant interventions to promote rehabilitation.
MeSH term(s)	Animals ; Humans ; Axons/metabolism ; Demyelinating Diseases/metabolism ; Myelin Sheath/metabolism ; Neuroprotection ; Oligodendroglia/metabolism ; Clinical Trials as Topic
Language	English
Publishing date	2023-11-22
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	639035-3
ISSN	2191-0200 ; 0334-1763
ISSN (online)	2191-0200
ISSN	0334-1763
DOI	10.1515/revneuro-2023-0081
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Article ; Online: Neuroserpin gene therapy inhibits retinal ganglion cell apoptosis and promotes functional preservation in glaucoma.

Chitranshi, Nitin / Rajput, Rashi / Godinez, Angela / Pushpitha, Kanishka / Mirzaei, Mehdi / Basavarajappa, Devaraj / Gupta, Veer / Sharma, Samridhi / You, Yuyi / Galliciotti, Giovanna / Salekdeh, Ghasem H / Baker, Mark S / Graham, Stuart L / Gupta, Vivek K

Molecular therapy : the journal of the American Society of Gene Therapy

2023 Volume 31, Issue 7, Page(s) 2056–2076

Abstract: Our research has proven that the inhibitory activity of the serine protease inhibitor neuroserpin (NS) is impaired because of its oxidation deactivation in glaucoma. Using genetic NS knockout ( ... ...

Abstract	Our research has proven that the inhibitory activity of the serine protease inhibitor neuroserpin (NS) is impaired because of its oxidation deactivation in glaucoma. Using genetic NS knockout (NS
MeSH term(s)	Mice ; Animals ; Retinal Ganglion Cells/metabolism ; Beclin-1/metabolism ; Disease Models, Animal ; Glaucoma/genetics ; Glaucoma/therapy ; Glaucoma/metabolism ; Apoptosis/genetics ; Intraocular Pressure ; Neuroserpin
Chemical Substances	Beclin-1
Language	English
Publishing date	2023-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2023.03.008
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Article ; Online: Corrigendum to - Chitosan modified 5-fluorouracil nanostructured lipid carriers for treatment of diabetic retinopathy in rats: A new dimension to an anticancer drug, Vol. 224, 1 January 2023, Pages 810-830.

International journal of biological macromolecules

2024 Volume 265, Issue Pt 2, Page(s) 131069

Language	English
Publishing date	2024-03-28
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	282732-3
ISSN	1879-0003 ; 0141-8130
ISSN (online)	1879-0003
ISSN	0141-8130
DOI	10.1016/j.ijbiomac.2024.131069
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Article ; Online: Neuroprotective Effects of Neuropeptide Y on Human Neuroblastoma SH-SY5Y Cells in Glutamate Excitotoxicity and ER Stress Conditions.

Palanivel, Viswanthram / Gupta, Vivek / Mirshahvaladi, Seyed Shahab Oddin / Sharma, Samridhi / Gupta, Veer / Chitranshi, Nitin / Mirzaei, Mehdi / Graham, Stuart L / Basavarajappa, Devaraj

Cells

2022 Volume 11, Issue 22

Abstract: Neuropeptide Y (NPY), a sympathetic neurotransmitter, is involved in various physiological functions, and its dysregulation is implicated in several neurodegenerative diseases. Glutamate excitotoxicity, endoplasmic reticulum (ER) stress, and oxidative ... ...

Abstract	Neuropeptide Y (NPY), a sympathetic neurotransmitter, is involved in various physiological functions, and its dysregulation is implicated in several neurodegenerative diseases. Glutamate excitotoxicity, endoplasmic reticulum (ER) stress, and oxidative stress are the common mechanisms associated with numerous neurodegenerative illnesses. The present study aimed to elucidate the protective effects of NPY against glutamate toxicity and tunicamycin-induced ER stress in the human neuroblastoma SH-SY5Y cell line. We exposed the SH-SY5Y cells to glutamate and tunicamycin for two different time points and analyzed the protective effects of NPY at different concentrations. The protective effects of NPY treatments were assessed by cell viability assay, and the signalling pathway changes were evaluated by biochemical techniques such as Western blotting and immunofluorescence assays. Our results showed that treatment of SH-SY5Y cells with NPY significantly increased the viability of the cells in both glutamate toxicity and ER stress conditions. NPY treatments significantly attenuated the glutamate-induced pro-apoptotic activation of ERK1/2 and JNK/BAD pathways. The protective effects of NPY were further evident against tunicamycin-induced ER stress. NPY treatments significantly suppressed the ER stress activation by downregulating BiP, phospho-eIF2α, and CHOP expression. In addition, NPY alleviated the Akt/FoxO3a pathway in acute oxidative conditions caused by glutamate and tunicamycin in SH-SY5Y cells. Our results demonstrated that NPY is neuroprotective against glutamate-induced cell toxicity and tunicamycin-induced ER stress through anti-apoptotic actions.
MeSH term(s)	Humans ; Neuroprotective Agents/pharmacology ; Neuropeptide Y/pharmacology ; Neuroblastoma ; Glutamic Acid/toxicity ; Tunicamycin/pharmacology ; Cell Line, Tumor
Chemical Substances	Neuroprotective Agents ; Neuropeptide Y ; Glutamic Acid (3KX376GY7L) ; Tunicamycin (11089-65-9)
Language	English
Publishing date	2022-11-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11223665
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Article: Oxidative Stress Induced Dysfunction of Protein Synthesis in 661W Mice Photoreceptor Cells.

Deng, Liting / Gupta, Vivek / Abyadeh, Morteza / Chitranshi, Nitin / Pushpitha, Kanishka / Wu, Yunqi / Gupta, Veer / You, Yuyi / Paulo, Joao A / Graham, Stuart L / Mirzaei, Mehdi / Haynes, Paul A

Proteomes

2023 Volume 11, Issue 2

Abstract: Photoreceptor cells are highly susceptible to oxidative-stress-induced damage due to their high metabolic rate. Oxidative stress plays a key role in driving pathological events in several different ocular diseases, which lead to retinal degeneration and ... ...

Abstract	Photoreceptor cells are highly susceptible to oxidative-stress-induced damage due to their high metabolic rate. Oxidative stress plays a key role in driving pathological events in several different ocular diseases, which lead to retinal degeneration and ultimately blindness. A growing number of studies have been performed to understand downstream events caused by ROS induced oxidative stress in photoreceptor cells; however, the underlying mechanisms of ROS toxicity are not fully understood. To shed light on ROS induced downstream pathological events, we employed a tandem mass tag (TMT) labelling-based quantitative mass-spectrometric approach to determine proteome changes in 661W photoreceptor cells following oxidative stress induction via the application of different concentrations of H
Language	English
Publishing date	2023-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720995-7
ISSN	2227-7382
ISSN	2227-7382
DOI	10.3390/proteomes11020012
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