Self-cytoprotection against stress: feedback regulation of heme-dependent metabolism

Schwartsburd, Polina

doi:10.1379/1466-1268(2001)006<0001:scasfr>2.0.co;2

Cited by 9 publications

(5 citation statements)

References 49 publications

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“…These results are in accord with a recent work of Oba et al (2015) who found that in mice, RIPC produced by ischemia/reperfusion of a hind limb, reduced infarct size and increased serum erythropoietin, which would reduce porphyrin level (Thunell, 2000). It also has been shown that chronic hypoxia triggers a large and abnormal laser-induced porphyrin auto fluorescent signal from tissues (Litvinova et al, 2009) whilst stress tolerance is associated with attenuation of the level of porphyrin due to coordinated negative feedback reactions involving inhibition of hemeoxygenase 1 and 5-aminolevulinic acid synthase (Schwartsburd, 2001; Papasimakis and Pallikari, 2010; Papaioannou et al, 2013; Rolf, 1998). Consequently, reduction in porphyrin autofluorescence in our study is another confirmation of increased stress resistance induced by RIPC in young healthy subjects and this metabolic change is likely to be mediated by ANS (Oba et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Metabolic stress (e.g. chronic hypoxia) is associated with increase in laser-induced porphyrin fluorescence (Litvinova et al, 2009) whilst a positive resistance to stress is characterized by reduced level of porphyrin in the aerobic cells (Schwartsburd, 2001). It should be noted, that there might be differences between the level of metabolites and proteins in the fingertip and in the central blood vessels (Nishiumi et al, 2019).…”

Section: Methodsmentioning

confidence: 99%

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Neuro-autonomic changes induced by remote ischemic preconditioning (RIPC) in healthy young adults: Implications for stress

Khaliulin

Fleishman

Шумейко

et al. 2019

Neurobiology of Stress

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The mechanisms underlying the protective effects of remote ischemic preconditioning (RIPC) are not presently clear. Recent studies in experimental models suggest the involvement of the autonomic nervous system (ANS) in cardioprotection. The aim of this study was to investigate the changes in ANS in healthy young volunteers divided into RIPC (n = 22) or SHAM (n = 18) groups. RIPC was induced by 1 cycle of 4 min inflation/5 min deflation followed by 2 cycles of 5 min inflation/5 min deflation of a cuff placed on the upper left limb. The study included analysis of heart rate (HR), blood pressure (BP), heart rate variability (HRV), measurements of microcirculation and porphyrin fluorescence in the limb before and after the RIPC. RIPC caused reactive hyperemia in the limb and reduced blood porphyrin level. A mental load (serial sevens test) and mild motor stress (hyperventilation) were performed on all subjects before and after RIPC or corresponding rest in the SHAM group. Reduction of HR occurred during the experiments in both RIPC and SHAM groups reflecting RIPC-independent adaptation of the subjects to the experimental procedure. However, in contrast to the SHAM group, RIPC altered several of the spectral indices of HRV during the serial sevens test and hyperventilation. This was expressed predominantly as an increase in power of the very low-frequency band of the spectrum, increased values of detrended fluctuation analysis and weakening of correlation between the HRV parameters and HR. In conclusion, RIPC induces changes in the activity of ANS that are linked to stress resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Neuro-autonomic changes induced by remote ischemic preconditioning (RIPC) in healthy young adults: Implications for stress

Khaliulin

Fleishman

Шумейко

et al. 2019

Neurobiology of Stress

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“…Ferrochelatase often is the rate‐limiting step for porphyrin production; hence, an increase in ferrochelatase indicates an increased demand in porphyrin [22]. Heme oxygenase‐1 catalyzes the decomposition of heme to biliverdin, carbon monoxide, and ferrous iron [23]. Biliverdin is further catalyzed to bilirubin, which is a powerful lipophilic antioxidant [24].…”

Section: Discussionmentioning

confidence: 99%

Cellular physiological effects of the MV Kyowa violet fuel‐oil spill on the hard coral, Porites lobata

Downs

Richmond

Mendiola

et al. 2006

Enviro Toxic and Chemistry

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The grounding of the Merchant Vessel (MV) Kyowa Violet on a coral reef near Yap, Federated States of Micronesia, in December 2002 resulted in the release of an estimated 55,000 to 80,000 gallons of intermediate fuel oil grade 180. The immediate impact was the widespread coating of mangroves and the intertidal zone along more than 8 km of coastline. Of greater concern, however, was the partitioning of the fuel oil in the water column, leading to chronic exposure of organisms in the ecosystem for a considerable period after the initial event. Herein, we report on our examination of one coral species, Porites lobata, nearly three months after the initial exposure. We investigated whether changes in cellular physiology were consistent with the pathological profile that results from the interaction of corals with polycyclic aromatic hydrocarbons, the principal constituent of fuel oil. Specifically, we document, to our knowledge for the first time, changes in the cellular physiological condition of an exposed coral population affected by a fuel-oil spill. We also provide evidence that the observed changes are consistent with a recent exposure to fuel oil, as evidenced by the presence of characteristic cellular lesions attributed to polycyclic aromatic hydrocarbons. Finally, our data support a model for a mechanistic relationship between the cellular pathological profile of the coral and a recent petroleum exposure, such as the MV Kyowa Violet fuel oil spill.

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“…In this work, we focused on negative feedback in yeast hypoxia regulation motivated by the extensive evidence for feedback in oxygen response pathways across biology (18,19). We characterized the feedback loop at the yeast hypoxia regulator ROX1 in molecular detail, and we harnessed this system as a test bed to study how feedback confers stability against naturally occurring mutations.…”

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confidence: 99%

Negative feedback confers mutational robustness in yeast transcription factor regulation

Denby

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Organismal fitness depends on the ability of gene networks to function robustly in the face of environmental and genetic perturbations. Understanding the mechanisms of this stability is one of the key aims of modern systems biology. Dissecting the basis of robustness to mutation has proven a particular challenge, with most experimental models relying on artificial DNA sequence variants engineered in the laboratory. In this work, we hypothesized that negative regulatory feedback could stabilize gene expression against the disruptions that arise from natural genetic variation. We screened yeast transcription factors for feedback and used the results to establish ROX1 (Repressor of hypOXia) as a model system for the study of feedback in circuit behaviors and its impact across genetically heterogeneous populations. Mutagenesis experiments revealed the mechanism of Rox1 as a direct transcriptional repressor at its own gene, enabling a regulatory program of rapid induction during environmental change that reached a plateau of moderate steady-state expression. Additionally, in a given environmental condition, Rox1 levels varied widely across genetically distinct strains; the ROX1 feedback loop regulated this variation, in that the range of expression levels across genetic backgrounds showed greater spread in ROX1 feedback mutants than among strains with the ROX1 feedback loop intact. Our findings indicate that the ROX1 feedback circuit is tuned to respond to perturbations arising from natural genetic variation in addition to its role in induction behavior. We suggest that regulatory feedback may be an important element of the network architectures that confer mutational robustness across biology.R obustness of organismal function in the face of perturbations is critical for fitness. Since the seminal work of Waddington (1), biologists have remarked on the stability of phenotypes against environmental and genetic variation, and understanding how organisms achieve robustness remains one of the major challenges in systems biology (2-4). Much of the search for molecular mechanisms of robustness has focused on gene regulation. Characteristics of regulatory networks that confer robustness include pathway redundancy and master regulatory organization (5), phenotypic capacitors (6-8), paired activating and inhibiting inputs (9), and cooperative and feed-forward regulation (10). Additionally, negative regulatory feedback, in which a biomolecule represses its own abundance, can buffer variation in gene expression (11,12), and negative feedback loops have been shown to underlie robustness to variable environmental conditions and stochastic intracellular change (13-15). Negative feedback may also confer network stability against the effects of mutations (3, 16), but evidence for negative feedback as a driver of mutational robustness in vivo has been at a premium (17); the relevance of this principle to natural genetic variation remains largely unknown.In this work, we focused on negative feedback in yeast hypoxia regulation motiva...

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Self-cytoprotection against stress: feedback regulation of heme-dependent metabolism

Cited by 9 publications

References 49 publications

Neuro-autonomic changes induced by remote ischemic preconditioning (RIPC) in healthy young adults: Implications for stress

Neuro-autonomic changes induced by remote ischemic preconditioning (RIPC) in healthy young adults: Implications for stress

Cellular physiological effects of the MV Kyowa violet fuel‐oil spill on the hard coral, Porites lobata

Negative feedback confers mutational robustness in yeast transcription factor regulation

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