Cellular Apoptosis and Organ Injury in Sepsis: A Review

Power, Colm; Fanning, Noel; Redmond, H. P.

doi:10.1097/00024382-200209000-00001

Cited by 82 publications

(61 citation statements)

References 130 publications

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“…Some of the changes such as cell shrinkage, chromatin condensation, or nuclear differences could be observed by microscopic techniques [1,7]. Morphological event cascade including cytoplasmic filament aggregation, nuclear condensation, cellular fragmentation, and plasma membrane blebbing finally results in the formation of apoptotic bodies.…”

Section: Morphological and Biochemical Processes Of Apoptosismentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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Section: Morphological and Biochemical Processes Of Apoptosismentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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“…It is well-known that during sepsis in animals and in vitro, bacterial endotoxins significantly inhibit apoptosis of neutrophils, which leads to clearance disturbance and may induce inflammation (Power et al 2002). Therefore, in the fourth series of experiments, we monitored the effect of rHsp70 preparations on normal neutrophil apoptosis after LTA addition.…”

Section: Hsp70 Pretreatment Does Not Significantly Modify Lta-inducedmentioning

confidence: 99%

Recombinant human Hsp70 protects against lipoteichoic acid-induced inflammation manifestations at the cellular and organismal levels

Винокуров

Ostrov

Yurinskaya

et al. 2012

Cell Stress and Chaperones

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It has been previously reported that pretreatment with exogenous heat shock protein 70 (Hsp70) is able to protect cells and animals from the deleterious effects of bacterial lipopolysaccharide (LPS) produced by Gramnegative bacteria. However, the effects of Hsp70 pretreatment on lipoteichoic acid (LTA) challenge resulted from Gram-positive bacteria infection have not been fully elucidated. In this study, we demonstrated that preconditioning with human recombinant Hsp70 ameliorates various manifestations of systematic inflammation, including reactive oxygen species, TNFα, and CD11b/CD18 adhesion receptor expression induction observed in different myeloid cells after LTA addition. Therefore, exogenous Hsp70 may provide a mechanism for controlling excessive inflammatory responses after macrophage activation. Furthermore, in a rat model of LTA-induced sepsis, we demonstrated that prophylactic administration of exogenous human Hsp70 significantly exacerbated numerous homeostatic and hemodynamic disturbances induced by LTA challenge and partially normalized the coagulation system and multiple biochemical blood parameters, including albumin and bilirubin concentrations, which were severely disturbed after LTA injections. Importantly, prophylactic intravenous injection of Hsp70 before LTA challenge significantly reduced mortality rates. Thus, exogenous mammalian Hsp70 may serve as a powerful cellular defense agent against the deleterious effects of bacterial pathogens, such as LTA and LPS. Taken together, our findings reveal novel functions of this protein and establish exogenous Hsp70 as a promising pharmacological agent for the prophylactic treatment of various types of sepsis.

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“…Free oxygen radicals and superoxide radicals cause endothelial damage, increased microvascular permeability, and tissue edema during reperfusion (2)(3)(4). As a result, cell membrane permeability decreases and, depending on the ischemia/reperfusion (I/R) time, apoptosis and necrosis develop (5).…”

Section: Introductionmentioning

confidence: 99%

Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

Topaloğlu¹,

Memi²,

Kaner³

et al. 2015

Turk J Med Sci

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Background/aim: To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats.Materials and methods: Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.Results: MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV. Conclusion:Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue.

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Cellular Apoptosis and Organ Injury in Sepsis: A Review

Cited by 82 publications

References 130 publications

Major apoptotic mechanisms and genes involved in apoptosis

Major apoptotic mechanisms and genes involved in apoptosis

Recombinant human Hsp70 protects against lipoteichoic acid-induced inflammation manifestations at the cellular and organismal levels

Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

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