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Special Issue "Molecular and Cellular Mechanisms of Action of Markers of Tissue Degeneration"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 28 February 2021.

Special Issue Editors

Prof. Dr. Carlos Gutierrez-Merino

Guest Editor
Professor of Biochemistry and Molecular Biology, Department of Biochemistry and Molecular Biology, Faculty of Sciences, and Institute of Molecular Pathology Biomarkers, University of Extremadura, Badajoz, Spain
Prof. Dr. Ana M. Mata

Co-Guest Editor
Departamento de Bioquímica y Biología Molecular y Genética, Facultad de Ciencias, Universidad de Extremadura and Instituto de Biomarcadores de Patologías Moleculares, Universidad de Extremadura, 06006 Badajoz, Spain

Special Issue Information

Dear Colleagues,

Mammalian tissue degeneration plays a major role either at the onset or in the early stages of many chronic diseases and insults to human health. A common feature of these threats to human health is that they initially develop slowly until tissue degeneration reaches an irreversible critical point. This critical point is currently associated with the activation of the proteases inducing cell death by apoptosis, necrosis or lysosomal dysfunction (including autophagocytosis).  

Studies of the molecular mechanisms underlying the biological dysregulation at the early and yet reversible stage of mammalian tissue degeneration are providing relevant clues to the most relevant molecular events triggering entry into the irreversible stage. The current knowledge points out that this early stage is a complex and multifactorial process induced by endogenous factors or exposure to drugs or environmental toxins that in most cases produce tissue inflammation, sustained cellular oxidative stress, and bioenergetic and cellular signaling dysregulation. Thus, there is a need to evaluate the relative contribution of different putative molecular mechanisms of dysregulation in each particular case, as well as the temporal sequence of molecular events that can lead to entry into the irreversible stage of tissue degeneration. Therefore, research on these molecular mechanisms is providing the most relevant biomarkers and biological targets for early diagnosis of the disease and/or for the design of rational therapeutic approaches to slow down or attenuate the severity of the health damage.

It is the aim of this Special Issue to focus on recent advances in the molecular mechanisms of biological dysregulation in the early and yet reversible stage of mammalian tissue degeneration.

Prof. Dr. Carlos Gutierrez-Merino
Prof. Dr. Ana M. Mata
Guest Editor

Manuscript Submission Information

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Published Papers (4 papers)

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Research

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Open AccessArticle
Early Reactive A1 Astrocytes Induction by the Neurotoxin 3-Nitropropionic Acid in Rat Brain
Int. J. Mol. Sci. 2020, 21(10), 3609; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21103609 - 20 May 2020
Cited by 1
Abstract
3-Nitropropionic acid (NPA) administration to rodents produces degeneration of the striatum, accompanied by neurological disturbances that mimic Huntington’s disease (HD) motor neurological dysfunctions. It has been shown that inflammation mediates NPA-induced brain degeneration, and activated microglia secreting cytokines interleukin-1α (IL-1α) and tumor [...] Read more.
3-Nitropropionic acid (NPA) administration to rodents produces degeneration of the striatum, accompanied by neurological disturbances that mimic Huntington’s disease (HD) motor neurological dysfunctions. It has been shown that inflammation mediates NPA-induced brain degeneration, and activated microglia secreting cytokines interleukin-1α (IL-1α) and tumor necrosis factor α (TNFα) can induce a specific type of reactive neurotoxic astrocytes, named A1, which have been detected in post-mortem brain samples of Huntington’s, Alzheimer’s, and Parkinson’s diseases. In this work we used an experimental model based on the intraperitoneal (i.p.) administration of NPA to adult Wistar rats at doses that can elicit extensive brain degeneration, and brain samples were taken before and after extensive brain damage monitored using 2,3,5-triphenyltetrazolium chloride (TTC) staining. Western blots and immunohistochemistry of brain slices show that i.p. NPA injections elicit significant increase in the expression levels of C3α subunit, a marker of generation of neurotoxic A1 astrocytes, and of cytokines IL-1α, TNFα, and C1q within the striatum, hippocampus, and cerebellum before the appearance of the HD-related neurological dysfunctions and neuronal death induced by NPA. Noteworthy, NPA administration primarily induces the generation of A1 astrocytes in the more recent phylogenetic area of the rat cerebellum. We conclude that the activation of complement C3 protein in the brain from Wistar rats is an early event in NPA-induced brain neurodegeneration. Full article
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Open AccessArticle
Age-Induced Differential Changes in the Central and Colonic Human Circadian Oscillators
Int. J. Mol. Sci. 2020, 21(2), 674; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21020674 - 20 Jan 2020
Cited by 1
Abstract
Aging modifies not only multiple cellular and homeostatic systems, but also biological rhythms. The circadian system is driven by a central hypothalamic oscillator which entrains peripheral oscillators, in both cases underlain by circadian genes. Our aim was to characterize the effect of aging [...] Read more.
Aging modifies not only multiple cellular and homeostatic systems, but also biological rhythms. The circadian system is driven by a central hypothalamic oscillator which entrains peripheral oscillators, in both cases underlain by circadian genes. Our aim was to characterize the effect of aging in the circadian expression of clock genes in the human colon. Ambulatory recordings of the circadian rhythms of skin wrist temperature, motor activity and the integrated variable TAP (temperature, activity and position) were dampened by aging, especially beyond 74 years of age. On the contrary, quantitative analysis of genes expression in the muscle layer of colonic explants during 24 h revealed that the circadian expression of Bmal1, Per1 and Clock genes, was larger beyond that age. In vitro experiments showed that aging induced a parallel increase in the myogenic contractility of the circular colonic muscle. This effect was not accompanied by enhancement of Ca2+ signals. In conclusion, we describe here for the first time the presence of a molecular oscillator in the human colon. Aging has a differential effect on the systemic circadian rhythms, that are impaired by aging, and the colonic oscillator, that is strengthened in parallel with the myogenic contractility. Full article
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Review

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Open AccessReview
Protein Biomarkers for the Diagnosis of Alzheimer’s Disease at Different Stages of Neurodegeneration
Int. J. Mol. Sci. 2020, 21(18), 6749; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186749 - 15 Sep 2020
Cited by 1
Abstract
Mainly obtained from familial Alzheimer’s disease patients’ data, we know that some features of the neurodegenerative start several years before the appearance of clinical symptoms. In this brief review, we comment on some molecular and cellular markers appearing at different stages of the [...] Read more.
Mainly obtained from familial Alzheimer’s disease patients’ data, we know that some features of the neurodegenerative start several years before the appearance of clinical symptoms. In this brief review, we comment on some molecular and cellular markers appearing at different stages of the disease, before or once the clinical symptoms are evident. These markers are present in biological fluids or could be identified by image techniques. The combined use of molecular and cellular markers will be of interest to determine the development of the different phases of the disease. Full article
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Open AccessReview
The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer′s Disease (AD)
Int. J. Mol. Sci. 2019, 20(19), 4661; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20194661 - 20 Sep 2019
Cited by 11
Abstract
Although the causative role of the accumulation of amyloid β 1–42 (Aβ42) deposits in the pathogenesis of Alzheimer′s disease (AD) has been under debate for many years, it is supposed that the toxicity soluble oligomers of Tau protein (TauOs) might be also the [...] Read more.
Although the causative role of the accumulation of amyloid β 1–42 (Aβ42) deposits in the pathogenesis of Alzheimer′s disease (AD) has been under debate for many years, it is supposed that the toxicity soluble oligomers of Tau protein (TauOs) might be also the pathogenic factor acting on the initial stages of this disease. Therefore, we performed a thorough search for literature pertaining to our investigation via the MEDLINE/PubMed database. It was shown that soluble TauOs, especially granular forms, may be the most toxic form of this protein. Hyperphosphorylated TauOs can reduce the number of synapses by missorting into axonal compartments of neurons other than axon. Furthermore, soluble TauOs may be also responsible for seeding Tau pathology within AD brains, with probable link to AβOs toxicity. Additionally, the concentrations of TauOs in the cerebrospinal fluid (CSF) and plasma of AD patients were higher than in non-demented controls, and revealed a negative correlation with mini-mental state examination (MMSE) scores. It was postulated that adding the measurements of TauOs to the panel of CSF biomarkers could improve the diagnosis of AD. Full article
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