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Article ; Online: Dopamine-loaded chitosan-coated solid lipid nanoparticles as a promise nanocarriers to the CNS.

Ortega Martínez, Elena / Morales Hernández, Ma Encarnación / Castillo-González, Julia / González-Rey, Elena / Ruiz Martínez, Ma Adolfina

Neuropharmacology

2024 Volume 249, Page(s) 109871

Abstract: Dopamine is unable to access the central nervous system through the bloodstream. Only its precursor can do so, and with an effectiveness below 100% of the dose administered, as it is metabolized before crossing the blood-brain barrier. In this study, we ... ...

Abstract	Dopamine is unable to access the central nervous system through the bloodstream. Only its precursor can do so, and with an effectiveness below 100% of the dose administered, as it is metabolized before crossing the blood-brain barrier. In this study, we describe a new solid lipid nanocarrier system designed and developed for dopamine. The nanoparticles were prepared by the melt-emulsification method and then coated with chitosan. The nanocarriers developed had a droplet size of about 250 nm, a polydispersity index of 0.2, a positive surface charge (+30 mV), and a percentage encapsulation efficiency of 36.3 ± 5.4. Transmission and scanning electron microscopy verified uniformity of particle size with spherical morphology. Various types of tests were performed to confirm that the nanoparticles designed are suitable for carrying dopamine through the blood-brain barrier. In vitro tests demonstrated the ability of these nanocarriers to pass through endothelial cell monolayers without affecting their integrity. This study shows that the formulation of dopamine in chitosan-coated solid lipid nanoparticles is a potentially viable formulation strategy to achieve the bioavailability of the drug for the treatment of Parkinson's disease in the central nervous system.
MeSH term(s)	Drug Carriers/metabolism ; Dopamine/metabolism ; Chitosan/metabolism ; Blood-Brain Barrier/metabolism ; Nanoparticles ; Liposomes
Chemical Substances	Lipid Nanoparticles ; Drug Carriers ; Dopamine (VTD58H1Z2X) ; Chitosan (9012-76-4) ; Liposomes
Language	English
Publishing date	2024-02-25
Publishing country	England
Document type	Journal Article
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2024.109871
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Article ; Online: Novel Therapeutic Opportunities for Neurodegenerative Diseases with Mesenchymal Stem Cells: The Focus on Modulating the Blood-Brain Barrier.

Vargas-Rodríguez, Pablo / Cuenca-Martagón, Alejandro / Castillo-González, Julia / Serrano-Martínez, Ignacio / Luque, Raúl M / Delgado, Mario / González-Rey, Elena

International journal of molecular sciences

2023 Volume 24, Issue 18

Abstract: Neurodegenerative disorders encompass a broad spectrum of profoundly disabling situations that impact millions of individuals globally. While their underlying causes and pathophysiology display considerable diversity and remain incompletely understood, a ...

Abstract	Neurodegenerative disorders encompass a broad spectrum of profoundly disabling situations that impact millions of individuals globally. While their underlying causes and pathophysiology display considerable diversity and remain incompletely understood, a mounting body of evidence indicates that the disruption of blood-brain barrier (BBB) permeability, resulting in brain damage and neuroinflammation, is a common feature among them. Consequently, targeting the BBB has emerged as an innovative therapeutic strategy for addressing neurological disorders. Within this review, we not only explore the neuroprotective, neurotrophic, and immunomodulatory benefits of mesenchymal stem cells (MSCs) in combating neurodegeneration but also delve into their recent role in modulating the BBB. We will investigate the cellular and molecular mechanisms through which MSC treatment impacts primary age-related neurological conditions like Alzheimer's disease, Parkinson's disease, and stroke, as well as immune-mediated diseases such as multiple sclerosis. Our focus will center on how MSCs participate in the modulation of cell transporters, matrix remodeling, stabilization of cell-junction components, and restoration of BBB network integrity in these pathological contexts.
MeSH term(s)	Humans ; Blood-Brain Barrier/pathology ; Neurodegenerative Diseases/pathology ; Parkinson Disease/pathology ; Alzheimer Disease/pathology ; Mesenchymal Stem Cells/physiology
Language	English
Publishing date	2023-09-14
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/ijms241814117
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Article ; Online: Role of Cortistatin in the Stressed Immune System.

Delgado, Mario / Gonzalez-Rey, Elena

Frontiers of hormone research

2017 Volume 48, Page(s) 110–120

Abstract: The immune system is faced with the daunting job of defending the organism against invading pathogens, while at the same time preserving the body integrity and maintaining tolerance to its own tissues. Loss of self-tolerance compromises immune ... ...

Abstract	The immune system is faced with the daunting job of defending the organism against invading pathogens, while at the same time preserving the body integrity and maintaining tolerance to its own tissues. Loss of self-tolerance compromises immune homeostasis and leads to the onset of autoimmune disorders. The identification of endogenous factors that control immune tolerance and inflammation is a key goal for immunologists. Evidences from the last decade indicate that the neuropeptide cortistatin is one of the endogenous factors. Cortistatin is produced by immune cells and through its binding to various receptors, it exerts potent anti-inflammatory actions and participates in the maintenance of immune tolerance at multiple levels, especially in immunological disorders. Cortistatin emerges as a key element in the bidirectional communication between the neuroendocrine and immune systems aimed at regulating body homeostasis.
MeSH term(s)	Homeostasis/physiology ; Humans ; Immune System/physiology ; Immune System/physiopathology ; Immune Tolerance/physiology ; Neuropeptides/physiology ; Neurosecretory Systems/physiology
Chemical Substances	Neuropeptides ; cortistatin
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1662-3762 ; 0301-3073
ISSN (online)	1662-3762
ISSN	0301-3073
DOI	10.1159/000452910
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Article ; Online: Cortistatin as a Novel Multimodal Therapy for the Treatment of Parkinson's Disease.

Serrano-Martínez, Ignacio / Pedreño, Marta / Castillo-González, Julia / Ferraz-de-Paula, Viviane / Vargas-Rodríguez, Pablo / Forte-Lago, Irene / Caro, Marta / Campos-Salinas, Jenny / Villadiego, Javier / Peñalver, Pablo / Morales, Juan Carlos / Delgado, Mario / González-Rey, Elena

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: Parkinson's disease (PD) is a complex disorder characterized by the impairment of the dopaminergic nigrostriatal system. PD has duplicated its global burden in the last few years, becoming the leading neurological disability worldwide. Therefore, there ... ...

Abstract	Parkinson's disease (PD) is a complex disorder characterized by the impairment of the dopaminergic nigrostriatal system. PD has duplicated its global burden in the last few years, becoming the leading neurological disability worldwide. Therefore, there is an urgent need to develop innovative approaches that target multifactorial underlying causes to potentially prevent or limit disease progression. Accumulating evidence suggests that neuroinflammatory responses may play a pivotal role in the neurodegenerative processes that occur during the development of PD. Cortistatin is a neuropeptide that has shown potent anti-inflammatory and immunoregulatory effects in preclinical models of autoimmune and neuroinflammatory disorders. The goal of this study was to explore the therapeutic potential of cortistatin in a well-established preclinical mouse model of PD induced by acute exposure to the neurotoxin 1-methil-4-phenyl1-1,2,3,6-tetrahydropyridine (MPTP). We observed that treatment with cortistatin mitigated the MPTP-induced loss of dopaminergic neurons in the substantia nigra and their connections to the striatum. Consequently, cortistatin administration improved the locomotor activity of animals intoxicated with MPTP. In addition, cortistatin diminished the presence and activation of glial cells in the affected brain regions of MPTP-treated mice, reduced the production of immune mediators, and promoted the expression of neurotrophic factors in the striatum. In an in vitro model of PD, treatment with cortistatin also demonstrated a reduction in the cell death of dopaminergic neurons that were exposed to the neurotoxin. Taken together, these findings suggest that cortistatin could emerge as a promising new therapeutic agent that combines anti-inflammatory and neuroprotective properties to regulate the progression of PD at multiple levels.
MeSH term(s)	Animals ; Mice ; Parkinson Disease/drug therapy ; Neurotoxins ; Neuropeptides ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use
Chemical Substances	cortistatin ; Neurotoxins ; Neuropeptides ; Anti-Inflammatory Agents
Language	English
Publishing date	2024-01-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25020694
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Article ; Online: Therapeutic application of mesenchymal stromal cells in murine models of inflammatory bowel disease.

Gonzalez-Rey, Elena / Delgado, Mario

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

2014 Volume 1213, Page(s) 331–339

Abstract: Mesenchymal stromal cells (MSCs) are currently under investigation for the treatment of inflammatory bowel disease (IBD), including Crohn's disease. The models of colitis induced by intrarectal infusion of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or by ...

Abstract	Mesenchymal stromal cells (MSCs) are currently under investigation for the treatment of inflammatory bowel disease (IBD), including Crohn's disease. The models of colitis induced by intrarectal infusion of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or by oral administration of dextran sulfate sodium (DSS) in susceptible mouse strains have been commonly used as preclinical tools to demonstrate the efficiency of treatments with MSCs isolated from various sources. Both models are being and will be critical to improve MSC-based therapies in human IBD by assaying new pathways, therapeutic regimes and tissue targeting strategies. Here, we describe our experiences in the treatment of acute and chronic TNBS- and DSS-induced colitis with MSCs.
MeSH term(s)	Animals ; Cell- and Tissue-Based Therapy ; Disease Models, Animal ; Inflammatory Bowel Diseases/chemically induced ; Inflammatory Bowel Diseases/therapy ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/cytology ; Mice ; Treatment Outcome
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-1453-1_27
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Article ; Online: Inflammasomes NLRP3 and AIM2 in peri-implantitis: A cross-sectional study.

Galindo-Moreno, Pablo / Montalvo-Acosta, Saray / Martín-Morales, Natividad / Carrillo-Gálvez, Ana Belén / González-Rey, Elena / O'Valle, Francisco / Padial-Molina, Miguel

Clinical oral implants research

2023 Volume 34, Issue 12, Page(s) 1342–1353

Abstract: Background: Inflammasome components NLRP3 and AIM2 contribute to inflammation development by the activation of caspase-1 and IL-1β. They have not been yet evaluated in samples from patients with active peri-implantitis. Thus, the aim of the present ... ...

Abstract	Background: Inflammasome components NLRP3 and AIM2 contribute to inflammation development by the activation of caspase-1 and IL-1β. They have not been yet evaluated in samples from patients with active peri-implantitis. Thus, the aim of the present study is to analyze the expression of inflammasomes NLRP3 and AIM2 and subsequent caspase 1 and IL-1β assessing the microenvironment of leukocyte subsets in samples from patients with active peri-implantitis. Methods: Biopsies were collected from 33 implants in 21 patients being treated for peri-implantitis. Biopsies from gingival tissues from 15 patients with healthy periodontium were also collected for control. These tissues were evaluated through conventional histological stainings. Then, immunohistochemical detection was performed to analyze NLRP3, AIM2, caspase-1, and IL-1β and markers of different leukocyte subsets. PCR for inflammasomes and related genes was also done. Results: This manuscript reveals a high immunohistochemical and mRNA expression of NLRP3 and AIM2 inflammasomes, caspase-1, and IL-1β in biopsies collected from human peri-implantitis. The expression of the tested markers was significantly correlated with the increase in inflammatory infiltrate, probing depth, presence of biofilm, and bleeding on probing. In these peri-implantitis lesions, the area of biopsy tissue occupied by inflammatory infiltrate was intense while the area occupied by collagen was significantly lower. In comparison with periodontal healthy tissues, the inflammatory infiltrate was statistically significantly higher in the peri-implantitis biopsies and was mainly composed of plasma cells, followed by T and B lymphocytes. Conclusion: In human peri-implantitis, chronic inflammation can be explained in part by the action of IL-1β/caspase 1 induced through NLRP3 and AIM2 inflammasome activation.
MeSH term(s)	Humans ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Peri-Implantitis ; Cross-Sectional Studies ; Caspase 1/metabolism ; Inflammation ; Interleukin-1beta/analysis ; DNA-Binding Proteins/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Caspase 1 (EC 3.4.22.36) ; Interleukin-1beta ; AIM2 protein, human ; DNA-Binding Proteins
Language	English
Publishing date	2023-08-29
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1067626-0
ISSN	1600-0501 ; 0905-7161
ISSN (online)	1600-0501
ISSN	0905-7161
DOI	10.1111/clr.14174
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Article: Educating the immune system with endogenous neuropeptides.

Gonzalez-Rey, Elena

Regulatory peptides

2010 Volume 164, Issue 1, Page(s) 21

Language	English
Publishing date	2010-09-9
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	225685-x
ISSN	0167-0115
ISSN	0167-0115
DOI	10.1016/j.regpep.2010.07.140
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Article ; Online: Keeping the balance between immune tolerance and pathogen immunity with endogenous neuropeptides.

Gonzalez-Rey, Elena

Neuroimmunomodulation

2010 Volume 17, Issue 3, Page(s) 161–164

Abstract: Identification of the factors that regulate the immune tolerance and control the appearance of exacerbated inflammatory conditions is crucial for the development of new therapies of inflammatory and autoimmune diseases. Although much is known about the ... ...

Abstract	Identification of the factors that regulate the immune tolerance and control the appearance of exacerbated inflammatory conditions is crucial for the development of new therapies of inflammatory and autoimmune diseases. Although much is known about the molecular basis of initiating signals and pro-inflammatory chemical mediators in inflammation, it has only recently become apparent that endogenous stop signals are critical at early checkpoints within the temporal events of inflammation. Some neuropeptides and hormones that are produced during the ongoing inflammatory response have emerged as endogenous anti-inflammatory agents that participate in the regulation of the processes that ensure self-tolerance and/or inflammation resolution. We will examine the latest research findings, which indicate that neuropeptides participate in maintaining immune tolerance in two distinct ways: by regulating the balance between pro-inflammatory and anti-inflammatory factors, and by inducing the emergence of regulatory T cells with suppressive activity against autoreactive T cell effectors. We will also examine the role of some of these neuropeptides as mediators of innate defense acting as natural antimicrobial peptides. Both anti-inflammatory and pro-resolving neuropeptides have shown therapeutic potential for a variety of inflammatory and autoimmune disorders and could be used as biotemplates for the development of novel pharmacologic agents. From a physiological point of view, neuropeptides play a critical role in the innate-adaptive immune cross talk that allows survival.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/physiopathology ; Humans ; Immune Tolerance/immunology ; Immune Tolerance/physiology ; Immunity, Innate/immunology ; Inflammation/immunology ; Inflammation/physiopathology ; Neuroimmunomodulation/physiology ; Neuropeptides/physiology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Neuropeptides
Language	English
Publishing date	2010
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1184368-8
ISSN	1423-0216 ; 1021-7401
ISSN (online)	1423-0216
ISSN	1021-7401
DOI	10.1159/000258713
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Article ; Online: Cortistatin deficiency reveals a dysfunctional brain endothelium with impaired gene pathways, exacerbated immune activation, and disrupted barrier integrity.

Castillo-González, Julia / Ruiz, José Luis / Serrano-Martínez, Ignacio / Forte-Lago, Irene / Ubago-Rodriguez, Ana / Caro, Marta / Pérez-Gómez, Jesús Miguel / Benítez-Troncoso, Alejandro / Andrés-León, Eduardo / Sánchez-Navarro, Macarena / Luque, Raúl M / González-Rey, Elena

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 226

Abstract: Background: Brain activity governing cognition and behaviour depends on the fine-tuned microenvironment provided by a tightly controlled blood-brain barrier (BBB). Brain endothelium dysfunction is a hallmark of BBB breakdown in most neurodegenerative/ ... ...

Abstract	Background: Brain activity governing cognition and behaviour depends on the fine-tuned microenvironment provided by a tightly controlled blood-brain barrier (BBB). Brain endothelium dysfunction is a hallmark of BBB breakdown in most neurodegenerative/neuroinflammatory disorders. Therefore, the identification of new endogenous molecules involved in endothelial cell disruption is essential to better understand BBB dynamics. Cortistatin is a neuroimmune mediator with anti-inflammatory and neuroprotective properties that exerts beneficial effects on the peripheral endothelium. However, its role in the healthy and injured brain endothelium remains to be evaluated. Herein, this study aimed to investigate the potential function of endogenous and therapeutic cortistatin in regulating brain endothelium dysfunction in a neuroinflammatory/neurodegenerative environment. Methods: Wild-type and cortistatin-deficient murine brain endothelium and human cells were used for an in vitro barrier model, where a simulated ischemia-like environment was mimicked. Endothelial permeability, junction integrity, and immune response in the presence and absence of cortistatin were evaluated using different size tracers, immunofluorescence labelling, qPCR, and ELISA. Cortistatin molecular mechanisms underlying brain endothelium dynamics were assessed by RNA-sequencing analysis. Cortistatin role in BBB leakage was evaluated in adult mice injected with LPS. Results: The endogenous lack of cortistatin predisposes endothelium weakening with increased permeability, tight-junctions breakdown, and dysregulated immune activity. We demonstrated that both damaged and uninjured brain endothelial cells isolated from cortistatin-deficient mice, present a dysregulated and/or deactivated genetic programming. These pathways, related to basic physiology but also crucial for the repair after damage (e.g., extracellular matrix remodelling, angiogenesis, response to oxygen, signalling, and metabolites transport), are dysfunctional and make brain endothelial barrier lacking cortistatin non-responsive to any further injury. Treatment with cortistatin reversed in vitro hyperpermeability, tight-junctions disruption, inflammatory response, and reduced in vivo BBB leakage. Conclusions: The neuropeptide cortistatin has a key role in the physiology of the cerebral microvasculature and its presence is crucial to develop a canonical balanced response to damage. The reparative effects of cortistatin in the brain endothelium were accompanied by the modulation of the immune function and the rescue of barrier integrity. Cortistatin-based therapies could emerge as a novel pleiotropic strategy to ameliorate neuroinflammatory/neurodegenerative disorders with disrupted BBB.
MeSH term(s)	Mice ; Animals ; Humans ; Endothelial Cells/metabolism ; Blood-Brain Barrier/metabolism ; Brain/metabolism ; Endothelium ; Brain Diseases ; Neuropeptides/metabolism
Chemical Substances	cortistatin ; Neuropeptides
Language	English
Publishing date	2023-10-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02908-5
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Article ; Online: Robust In Vitro and In Vivo Immunosuppressive and Anti-inflammatory Properties of Inducible Caspase-9-mediated Apoptotic Mesenchymal Stromal/Stem Cell.

Romecín, Paola Alejandra / Vinyoles, Meritxell / López-Millán, Belén / de la Guardia, Rafael Diaz / Atucha, Noemi M / Querol, Sergi / Bueno, Clara / Benitez, Raquel / Gonzalez-Rey, Elena / Delgado, Mario / Menéndez, Pablo

Stem cells translational medicine

2022 Volume 11, Issue 1, Page(s) 88–96

Abstract: Mesenchymal stromal stem/cells (MSC) therapies are clinically used in a wide range of disorders based on their robust HLA-independent immunosuppressive and anti-inflammatory properties. However, the mechanisms underlying MSC therapeutic activity remain ... ...

Abstract	Mesenchymal stromal stem/cells (MSC) therapies are clinically used in a wide range of disorders based on their robust HLA-independent immunosuppressive and anti-inflammatory properties. However, the mechanisms underlying MSC therapeutic activity remain elusive as demonstrated by the unpredictable therapeutic efficacy of MSC infusions reported in multiple clinical trials. A seminal recent study showed that infused MSCs are actively induced to undergo apoptosis by recipient cytotoxic T cells, a mechanism that triggers in vivo recipient-induced immunomodulation by such apoptotic MSCs, and the need for such recipient cytotoxic cell activity could be replaced by the administration of ex vivo-generated apoptotic MSCs. Moreover, the use of MSC-derived extracellular vesicles (MSC-EVs) is being actively explored as a cell-free therapeutic alternative over the parental MSCs. We hypothesized that the introduction of a "suicide gene" switch into MSCs may offer on-demand in vivo apoptosis of transplanted MSCs. Here, we prompted to investigate the utility of the iCasp9/AP1903 suicide gene system in inducing apoptosis of MSCs. iCasp9/AP1903-induced apoptotic MSCs (MSCiCasp9+) were tested in vitro and in in vivo models of acute colitis. Our data show a very similar and robust immunosuppressive and anti-inflammatory properties of both "parental" alive MSCGFP+ cells and apoptotic MSCiCasp9+ cells in vitro and in vivo regardless of whether apoptosis was induced in vivo or in vitro before administering MSCiCasp9+ lysates. This development of an efficient iCasp9 switch may potentiate the safety of MSC-based therapies in the case of an adverse event and, will also circumvent current logistic technical limitations and biological uncertainties associated to MSC-EVs.
MeSH term(s)	Anti-Inflammatory Agents ; Caspase 9 ; Extracellular Vesicles/transplantation ; Humans ; Immunomodulation ; Immunosuppressive Agents ; Mesenchymal Stem Cells
Chemical Substances	Anti-Inflammatory Agents ; Immunosuppressive Agents ; Caspase 9 (EC 3.4.22.-)
Language	English
Publishing date	2022-01-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2642270-0
ISSN	2157-6580 ; 2157-6580
ISSN (online)	2157-6580
ISSN	2157-6580
DOI	10.1093/stcltm/szab007
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