Análisis comparativo de marcadores de lesión en modelos de isquemia cerebral focal y global en ratas

Céspedes, Ángel; Arango, César; Cardona, Gloria Patricia

doi:10.7705/biomedica.v33i2.830

Cited by 6 publications

(4 citation statements)

References 47 publications

(86 reference statements)

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“…Globally, astrocytes are characterized by the expression of the intermediate filaments vimentin (Vim) and glial fibrillary acidic protein (GFAP), which are upregulated under CNS insults, in a process known as astrogliosis (Volterra and Meldolesi, 2005 ; Hamby and Sofroniew, 2010 ; Céspedes et al, 2013 ). Morphologically, astrocytes are characterized by a stellate shape with multiple processes and ramifications (Chen and Swanson, 2003 ; Volterra and Meldolesi, 2005 ), and become activated following brain injuries and degenerative diseases (Barreto et al, 2007 , 2009 , 2011 , 2012 ; Adelson et al, 2012 ).…”

Section: Components Of the Bbbmentioning

confidence: 99%

Astrocytic modulation of blood brain barrier: perspectives on Parkinsonâ€™s disease

Cabezas

Ávila

González

et al. 2014

Front. Cell. Neurosci.

341

250

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The blood–brain barrier (BBB) is a tightly regulated interface in the Central Nervous System (CNS) that regulates the exchange of molecules in and out from the brain thus maintaining the CNS homeostasis. It is mainly composed of endothelial cells (ECs), pericytes and astrocytes that create a neurovascular unit (NVU) with the adjacent neurons. Astrocytes are essential for the formation and maintenance of the BBB by providing secreted factors that lead to the adequate association between the cells of the BBB and the formation of strong tight junctions. Under neurological disorders, such as chronic cerebral ischemia, brain trauma, Epilepsy, Alzheimer and Parkinson’s Diseases, a disruption of the BBB takes place, involving a lost in the permeability of the barrier and phenotypical changes in both the ECs and astrocytes. In this aspect, it has been established that the process of reactive gliosis is a common feature of astrocytes during BBB disruption, which has a detrimental effect on the barrier function and a subsequent damage in neuronal survival. In this review we discuss the implications of astrocyte functions in the protection of the BBB, and in the development of Parkinson’s disease (PD) and related disorders. Additionally, we highlight the current and future strategies in astrocyte protection aimed at the development of restorative therapies for the BBB in pathological conditions.

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Section: Components Of the Bbbmentioning

confidence: 99%

Astrocytic modulation of blood brain barrier: perspectives on Parkinsonâ€™s disease

Cabezas

Ávila

González

et al. 2014

Front. Cell. Neurosci.

341

250

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“…In recent studies, we found that glutamate-mediated excitotoxicity decreases the number and length of dendrites and induces tau hyperphosphorylation (Posada-Duque et al, 2013 ). The hyperphosphorylation of tau, a neurodegeneration marker, is also increased by global and transient focal cerebral ischemia, causing alterations in spatial memory (Castro-Alvarez et al, 2011 ; Céspedes et al, 2013 ). At the cellular level, hyperactivated GSK3 protein is associated with alterations in microtubule assembly, and the activity of RhoA has been associated with the retraction of the actin cytoskeleton (Céspedes-Rubio et al, 2010 ).…”

Section: Cerebral Ischemiamentioning

confidence: 99%

Protection after stroke: cellular effectors of neurovascular unit integrity

Posada‐Duque

Barreto

Cardona‐Gómez

2014

Front. Cell. Neurosci.

105

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Neurological disorders are prevalent worldwide. Cerebrovascular diseases (CVDs), which account for 55% of all neurological diseases, are the leading cause of permanent disability, cognitive and motor disorders and dementia. Stroke affects the function and structure of blood-brain barrier, the loss of cerebral blood flow regulation, oxidative stress, inflammation and the loss of neural connections. Currently, no gold standard treatments are available outside the acute therapeutic window to improve outcome in stroke patients. Some promising candidate targets have been identified for the improvement of long-term recovery after stroke, such as Rho GTPases, cell adhesion proteins, kinases, and phosphatases. Previous studies by our lab indicated that Rho GTPases (Rac and RhoA) are involved in both tissue damage and survival, as these proteins are essential for the morphology and movement of neurons, astrocytes and endothelial cells, thus playing a critical role in the balance between cell survival and death. Treatment with a pharmacological inhibitor of RhoA/ROCK blocks the activation of the neurodegeneration cascade. In addition, Rac and synaptic adhesion proteins (p120 catenin and N-catenin) play critical roles in protection against cerebral infarction and in recovery by supporting the neurovascular unit and cytoskeletal remodeling activity to maintain the integrity of the brain parenchyma. Interestingly, neuroprotective agents, such as atorvastatin, and CDK5 silencing after cerebral ischemia and in a glutamate-induced excitotoxicity model may act on the same cellular effectors to recover neurovascular unit integrity. Therefore, future efforts must focus on individually targeting the structural and functional roles of each effector of neurovascular unit and the interactions in neural and non-neural cells in the post-ischemic brain and address how to promote the recovery or prevent the loss of homeostasis in the short, medium and long term.

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“…Astrocytes are normal cells in the mammalian brain coinciding with oligodendrocytes and microglia [204]. The main feature of astrocytes is the expression of the intermediate filaments vimentin and glial fibrillary acidic protein (GFAP), which are upregulated during CNS injury, where the astrocytes become reactive in a process known as astrocytosis or astrogliosis [205–207]. The BBB is formed by brain capillary and endothelial cells (ECs) which are strongly associated with astrocyte endfeet processes and pericyte cells [138].…”

Section: Pathological Conditions Of Citrullinationmentioning

confidence: 99%

An Overview of the Intrinsic Role of Citrullination in Autoimmune Disorders

Alghamdi

Alasmari

Assiri

et al. 2019

Journal of Immunology Research

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A protein undergoes many types of posttranslation modification. Citrullination is one of these modifications, where an arginine amino acid is converted to a citrulline amino acid. This process depends on catalytic enzymes such as peptidylarginine deiminase enzymes (PADs). This modification leads to a charge shift, which affects the protein structure, protein-protein interactions, and hydrogen bond formation, and it may cause protein denaturation. The irreversible citrullination reaction is not limited to a specific protein, cell, or tissue. It can target a wide range of proteins in the cell membrane, cytoplasm, nucleus, and mitochondria. Citrullination is a normal reaction during cell death. Apoptosis is normally accompanied with a clearance process via scavenger cells. A defect in the clearance system either in terms of efficiency or capacity may occur due to massive cell death, which may result in the accumulation and leakage of PAD enzymes and the citrullinated peptide from the necrotized cell which could be recognized by the immune system, where the immunological tolerance will be avoided and the autoimmune disorders will be subsequently triggered. The induction of autoimmune responses, autoantibody production, and cytokines involved in the major autoimmune diseases will be discussed.

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Análisis comparativo de marcadores de lesión en modelos de isquemia cerebral focal y global en ratas

Cited by 6 publications

References 47 publications

Astrocytic modulation of blood brain barrier: perspectives on Parkinsonâ€™s disease

Astrocytic modulation of blood brain barrier: perspectives on Parkinsonâ€™s disease

Protection after stroke: cellular effectors of neurovascular unit integrity

An Overview of the Intrinsic Role of Citrullination in Autoimmune Disorders

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