Esophageal contraction during cryoablation: A possible protective mechanism

The structure of the laboratory population of green microalgae Scenedesmus quadricauda (Turp.) Breb (=Desmodesmus communis E. Hegew.) was studied at different stages of its growth (lag-phase, log-phase and stationary phase) at low concentrations of copper chloride and silver nitrate by the method microculture, allowing to monitor the state and development of single cells having different physiological status. The response of the culture of S. quadricauda - the change in the number of cells and the fractional composition (the fraction of dividing, «dormant» and dying cells) depended not only on the concentration of the toxicant in the medium, but also on the physiological state of the culture: the level of synchronization and the growth phase. Silver ions at low concentrations had a more pronounced toxic effect on the culture than copper ions at different phases of its development, especially at a concentration of 0.001 mg/l (10-9 M). The main mechanism of the toxic effect of metals is to inhibit the process of cell division. At low concentrations of toxicants, especially at a concentration of 0.001 mg/l, a «paradoxical» effect expressed in the predominance of the fraction of «dormant» cells was revealed. The temporary inhibition of the process of cell division can be regarded as a protective mechanism that allows preserving the integrity of the population and its ability to survive in a changing environment. The obtained data explain the effect of action of low concentrations of substances due to their inclusion in the cell, the subsequent accumulation in the cell and their low excretion.

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Inhibition of Autophagy Potentiated Hippocampal Cell Death Induced by Endoplasmic Reticulum Stress and its Activation by Trehalose Failed to be Neuroprotective

Current Neurovascular Research ◽

10.2174/1567202616666190131155834 ◽

2019 ◽

Vol 16 (1) ◽

pp. 3-11

Author(s):

Luisa Halbe ◽

Abdelhaq Rami

Keyword(s):

Endoplasmic Reticulum ◽

Cell Death ◽

Er Stress ◽

Cell Damage ◽

Protective Mechanism ◽

Unfolded Proteins ◽

Neuronal Viability ◽

Hippocampal Cell ◽

Trigger Cell Death ◽

Autophagy Inhibition

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.

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Daily Stimulation and Cognitive Functioning: The Importance of the Participation of Healthy Older People in Cognitively Demanding Everyday Activities

European Journal of Investigation in Health, Psychology and Education ◽

10.3390/ejihpe4030029 ◽

2014 ◽

Vol 4 (3) ◽

pp. 309-319

Author(s):

José Antonio Labra Pérez ◽

Julio Menor

Keyword(s):

Cognitive Functioning ◽

Urban Areas ◽

Ad Hoc ◽

The Elderly ◽

Protective Mechanism ◽

Everyday Activity ◽

Neuropsychological Measures ◽

Rural And Urban Areas ◽

Everyday Activities ◽

Rural And Urban

The participation of the elderly in cognitively demanding activities is considered an enhancing factor of cognitive function. However, the life cycle psychosocial variables such as education and type of profession also influence in cognitive functioning. The objective of this study is to analyze the relationship between daily stimulation and cognitive functioning in a sample of healthy older adults, controlling the effects of education and the type of profession. The study involved 164 adults over 60 years, from rural and urban areas, with different levels of education and professional level which were assessed with an extensive battery of neuropsychological measures, as well as in an inventory of everyday activities built ad hoc. The results show that different cognitively demanding everyday activities are related to with cognitive processes, both fluids and crystallized. Furthermore, it was found that daily stimulation plays an important role in cognitive functioning outside of education and the type of profession performed. Overall, the results of this study shows the importance of everyday activity as a protective mechanism against cognitive decline, as well as the need to adopt a model of active aging

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Roux-en-Y Gastric Bypass Downregulates Angiotensin-Converting Enzyme 2 (ACE2) Gene Expression in Subcutaneous White Adipose Tissue: A Putative Protective Mechanism Against Severe COVID-19

Obesity Surgery ◽

10.1007/s11695-021-05271-7 ◽

2021 ◽

Author(s):

Leonardo Kristem ◽

Mariana Recamonde-Mendoza ◽

Giuliano C. Cigerza ◽

Jad Khoraki ◽

Guilherme M. Campos ◽

...

Keyword(s):

Gene Expression ◽

Gastric Bypass ◽

Adipose Tissue ◽

Angiotensin Converting Enzyme ◽

White Adipose Tissue ◽

Protective Mechanism ◽

Converting Enzyme ◽

Angiotensin Converting Enzyme 2 ◽

Subcutaneous White Adipose Tissue ◽

Ace2 Gene

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Autophagy Deficiency by Atg4B Loss Leads to Metabolomic Alterations in Mice

Metabolites ◽

10.3390/metabo11080481 ◽

2021 ◽

Vol 11 (8) ◽

pp. 481

Author(s):

Gemma G. Martínez-García ◽

Raúl F. Pérez ◽

Álvaro F. Fernández ◽

Sylvere Durand ◽

Guido Kroemer ◽

...

Keyword(s):

Skeletal Muscle ◽

Amino Acids ◽

Mammalian Cells ◽

Tissue Homeostasis ◽

In Vivo Studies ◽

Protective Mechanism ◽

Cardiac Damage ◽

Wide Range ◽

First Time

Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals.

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Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

International Journal of Molecular Sciences ◽

10.3390/ijms22094646 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4646

Author(s):

Alexey A. Tinkov ◽

Monica M. B. Paoliello ◽

Aksana N. Mazilina ◽

Anatoly V. Skalny ◽

Airton C. Martins ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Mitochondrial Dysfunction ◽

Synaptic Dysfunction ◽

Future Research ◽

Protective Mechanism ◽

Autophagic Flux ◽

Future Research Directions ◽

The Impact

Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity.

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The Protective Mechanism of SIRT1 in the Regulation of Mitochondrial Biogenesis and Mitochondrial Autophagy in Alzheimer’s Disease

Journal of Alzheimer s Disease ◽

10.3233/jad-210132 ◽

2021 ◽

pp. 1-9

Author(s):

Fan Ye ◽

Anshi Wu

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mitochondrial Biogenesis ◽

Stress Responses ◽

Histone Deacetylases ◽

Neuronal Morphology ◽

Protective Mechanism ◽

Peroxisome Proliferator ◽

Class Iii ◽

Peroxisome Proliferator Activated Receptor

Silent information-regulated transcription factor 1 (SIRT1) is the most prominent and widely studied member of the sirtuins (a family of mammalian class III histone deacetylases). It is a nuclear protein, and the deacetylation of the peroxisome proliferator-activated receptor coactivator-1 has been extensively implicated in metabolic control and mitochondrial biogenesis and is the basis for studies into its involvement in caloric restriction and its effects on lifespan. The present study discusses the potentially protective mechanism of SIRT1 in the regulation of the mitochondrial biogenesis and autophagy involved in the modulation of Alzheimer’s disease, which may be correlated with the role of SIRT1 in affecting neuronal morphology, learning, and memory during development; regulating metabolism; counteracting stress responses; and maintaining genomic stability. Drugs that activate SIRT1 may offer a promising approach to treating Alzheimer’s disease

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EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response

Scientific Reports ◽

10.1038/s41598-021-90398-x ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Mian Wang ◽

Hua Zhong ◽

Xian Zhang ◽

Xin Huang ◽

Jing Wang ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Signaling Pathway ◽

Weight Ratio ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Protective Mechanism ◽

High Morbidity ◽

Inflammatory Factor ◽

Egcg Treatment

AbstractAcute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer properties, including epigallocatechin-3-gallate (EGCG). In the present study, protein kinase C alpha (PRKCA) is involved in EGCG protection against LPS-induced inflammation and ALI. EGCG treatment attenuated LPS-stimulated ALI in mice as manifested as improved lung injury scores, decreased total cell amounts, neutrophil amounts and macrophage amounts, inhibited the activity of MPO, decreased wet-to-dry weight ratio of lung tissues, and inhibited release of inflammatory cytokines TNF-α, IL-1β, and IL-6. PRKCA mRNA and protein expression showed to be dramatically decreased by LPS treatment while reversed by EGCG treatment. Within LPS-stimulated ALI mice, PRKCA silencing further aggravated, while PRKCA overexpression attenuated LPS-stimulated inflammation and ALI through MAPK signaling pathway. PRKCA silencing attenuated EGCG protection. Within LPS-induced RAW 264.7 macrophages, EGCG could induce PRKCA expression. Single EGCG treatment or Lv-PRKCA infection attenuated LPS-induced increases in inflammatory factors; PRKCA silencing could reverse the suppressive effects of EGCG upon LPS-stimulated inflammatory factor release. In conclusion, EGCG pretreatment inhibits LPS-induced ALI in mice. The protective mechanism might be associated with the inhibitory effects of PRKCA on proinflammatory cytokine release via macrophages and MAPK signaling pathway.

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