Heat Stress Induces Extended Plateau of Hsp70 Accumulation – A Possible Cytoprotection Mechanism in Hepatic Cells

Miova, Biljana; Dinevska-Ќovkarovska, Suzana; Esplugues, Juan V.; Apostolova, Nadezda

doi:10.1002/jcb.25187

Cited by 12 publications

(14 citation statements)

References 37 publications

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“…Nevertheless, a significantly lower HSP70 expression has been reported in 14d-versus 2d-diabetic animals, D r a f t which is in accordance with other reports showing that HSP72 synthesis flourishes in the first 24-48 following HS and declines later on (Horowitz 2003). In HepG2 cells, abundant level of HSP70 and BCl-2 was observed 24-48h after the single HS, which indicate that HS might be a "physiological conditioner" and might obtain cytoprotection against an additional stress (Miova et al 2015).…”

Section: Heat Preconditioning Of Diabetic Animalssupporting

confidence: 90%

“…The duration of diabetes in our experiment was defined by the following criteria: minimum period for manifestation of the effect of administrated STZ (48h) and optimal period for the development of diabetic complications (14 days); abundant HSP70 protein level in the first 24-48h after the single HS, and further decrement after the 72h after the HS [both in cells (Miova et al 2015) and in rats (Horowitz 2003)]. Experimental diabetes mellitus was induced by a single intraperitoneal injection of streptozotocin (STZ, 55 mg/kg body weight) and was freshly dissolved in 0.1M citrate buffer, pH=4.5.…”

Section: Study Design and Treatmentsmentioning

confidence: 99%

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Physiological and pharmacological inductors of HSP70 enhance the antioxidative defense mechanisms of the liver and pancreas in diabetic rats

Dimitrovska

Dervisevik

Cipanovska

et al. 2018

Can. J. Physiol. Pharmacol.

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Heat preconditioning (HP) is a powerful adaptive and protective phenomenon and the heat stress proteins (HSPs) it produces are an important determinant for the development of diabetic complications. Aspirin has been reported to modulate heat shock response in different organisms through increased induction of HSPs and is also known to exert antioxidative and radical scavenging effects in diabetes. We estimated the effect of physiological (heat stress: 45 min at 41 ± 0.5 °C) and pharmacological (aspirin treatment) induction of HSP70 on several parameters of oxidative state in the pancreas and liver of diabetic rats. Diabetes increased HSP70 level and decreased poly(ADP) ribose polymerase (PARP), glutathione (GSH), and glutathione peroxidase (GPx) activities in the pancreas. In the liver, there was reduction of HSP70 level, GSH concentration, and CAT activity, while GPx and GR activity were enhanced. HP of diabetic rats caused an additional increase of HSP70, GSH, and antioxidant enzymes in both organs. Pre-treatment of HP-diabetic animals with aspirin led to an additional increase of PARP and HSP70. Both HP and aspirin, as physiological and pharmacological inductors of HSP70, respectively, enhanced the antioxidative defense mechanisms of the liver and pancreas in diabetic rats.

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Section: Heat Preconditioning Of Diabetic Animalssupporting

confidence: 90%

Section: Study Design and Treatmentsmentioning

confidence: 99%

Physiological and pharmacological inductors of HSP70 enhance the antioxidative defense mechanisms of the liver and pancreas in diabetic rats

Dimitrovska

Dervisevik

Cipanovska

et al. 2018

Can. J. Physiol. Pharmacol.

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“…In addition, HSP70 regulates apoptotic signaling pathways in different manners, such as promoting or suppressing apoptosis [ 11 ]. In terms of apoptosis, there are two key players, the transcription factors Bcl-2 and p53, whose expression can be affected by HSP70 [ 14 ]. HSP70 also participates in the regulation of myocardial apoptosis after ischemia-reperfusion injury, neurodegeneration, and chronic diseases (e.g., diabetes and neurological disorders) [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Role of MAPKs in HSP70’s Protection against Heat Stress-Induced Injury in Rat Small Intestine

Hao

Feng

2018

BioMed Research International

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Aim To evaluate the role of heat shock protein 70 (HSP70) on the MAPK pathway activation with quercetin treatment and its protection against small intestine impairments of heat stressed rats. Methods Forty-eight male Sprague-Dawley rats aged 6 weeks were randomized to three groups (n=16/group), namely, control (CON), heat stress (HS), and heat stress + quercetin (HQ). The experiment lasted for 14 days with daily 50 min of heat stress treatment (43°C) for the HS and HQ groups. Rats of HQ group were intragastrically given 0.5 ml quercetin solution (50 mg/kg body weight) before the heat stress treatment. Half of the animals were sacrificed on day 7 and the rest on day 14 for tissue sampling. Intestinal morphology, small intestine morphology and permeability, protein expression of HSP70, phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and caspase-3 activity were examined. Results Heat stress caused morphological damage to the small intestine and increased intestinal permeability. HSP70 expression and MAPK activity in the small intestine were increased by heat stress. Inhibition of HSP70 by quercetin did not change intestinal permeability compared with the HS group but aggravated intestinal injury and affected the activation of MAPKs and caspase-3. Conclusions HSP70 may modulate stress-activated signaling and acts in a protective manner via MAPK signaling. Affecting HSP70 protective mechanisms could be useful for protection against heat stress-induced injury in rat small intestine.

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“…What is interesting is the apparent cyclical pattern of the results, suggesting a possible biphasic response in the liver at early time points after TBI. Previous in vitro and in vivo studies examining acute liver injury have demonstrated a biphasic hepatocyte response that may correspond to hepatocyte apoptosis and/or liver necrosis7071. Thus, it is possible that at later, or different time points than we examined, hedgehog and Gli signaling are increased, as the liver mobilizes immune cells and attempts to restore homeostatic function72.…”

Section: Discussionmentioning

confidence: 94%

Hepatic alterations are accompanied by changes to bile acid transporter-expressing neurons in the hypothalamus after traumatic brain injury

Nizamutdinov

DeMorrow

McMillin

et al. 2017

Sci Rep

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Annually, there are over 2 million incidents of traumatic brain injury (TBI) and treatment options are non-existent. While many TBI studies have focused on the brain, peripheral contributions involving the digestive and immune systems are emerging as factors involved in the various symptomology associated with TBI. We hypothesized that TBI would alter hepatic function, including bile acid system machinery in the liver and brain. The results show activation of the hepatic acute phase response by 2 hours after TBI, hepatic inflammation by 6 hours after TBI and a decrease in hepatic transcription factors, Gli 1, Gli 2, Gli 3 at 2 and 24 hrs after TBI. Bile acid receptors and transporters were decreased as early as 2 hrs after TBI until at least 24 hrs after TBI. Quantification of bile acid transporter, ASBT-expressing neurons in the hypothalamus, revealed a significant decrease following TBI. These results are the first to show such changes following a TBI, and are compatible with previous studies of the bile acid system in stroke models. The data support the emerging idea of a systemic influence to neurological disorders and point to the need for future studies to better define specific mechanisms of action.

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Heat Stress Induces Extended Plateau of Hsp70 Accumulation – A Possible Cytoprotection Mechanism in Hepatic Cells

Cited by 12 publications

References 37 publications

Physiological and pharmacological inductors of HSP70 enhance the antioxidative defense mechanisms of the liver and pancreas in diabetic rats

Physiological and pharmacological inductors of HSP70 enhance the antioxidative defense mechanisms of the liver and pancreas in diabetic rats

Role of MAPKs in HSP70’s Protection against Heat Stress-Induced Injury in Rat Small Intestine

Hepatic alterations are accompanied by changes to bile acid transporter-expressing neurons in the hypothalamus after traumatic brain injury

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