Differential expression of heat shock proteins 70-1 and 70-2 mRNA after ischemia-reperfusion injury of rat kidney

1999 ◽  
Vol 27 (5) ◽  
pp. 306-311 ◽  
Author(s):  
Ziya Akçetin ◽  
Reinhard Pregla ◽  
Dorothea Darmer ◽  
Hans Heynemann ◽  
Johannes Haerting ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Differential Expression ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Shock Proteins

scholarly journals Heat Shock Proteins in Oxidative Stress and Ischemia/Reperfusion Injury and Benefits from Physical Exercises: A Review to the Current Knowledge

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jakub Szyller ◽  
Iwona Bil-Lula
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Physical Exercises ◽  
Shock Proteins

Heat shock proteins (HSPs) are molecular chaperones produced in response to oxidative stress (OS). These proteins are involved in the folding of newly synthesized proteins and refolding of damaged or misfolded proteins. Recent studies have been focused on the regulatory role of HSPs in OS and ischemia/reperfusion injury (I/R) where reactive oxygen species (ROS) play a major role. ROS perform many functions, including cell signaling. Unfortunately, they are also the cause of pathological processes leading to various diseases. Biological pathways such as p38 MAPK, HSP70 and Akt/GSK-3β/eNOS, HSP70, JAK2/STAT3 or PI3K/Akt/HSP70, and HSF1/Nrf2-Keap1 are considered in the relationship between HSP and OS. New pathophysiological mechanisms involving ROS are being discovered and described the protein network of HSP interactions. Understanding of the mechanisms involved, e.g., in I/R, is important to the development of treatment methods. HSPs are multifunctional proteins because they closely interact with the antioxidant and the nitric oxide generation systems, such as HSP70/HSP90/NOS. A deficiency or excess of antioxidants modulates the activation of HSF and subsequent HSP biosynthesis. It is well known that HSPs are involved in the regulation of several redox processes and play an important role in protein-protein interactions. The latest research focuses on determining the role of HSPs in OS, their antioxidant activity, and the possibility of using HSPs in the treatment of I/R consequences. Physical exercises are important in patients with cardiovascular diseases, as they affect the expression of HSPs and the development of OS.

PRIOR INDUCTION OF HEAT SHOCK PROTEINS BY A NITRIC OXIDE DONOR ATTENUATES CARDIAC ISCHEMIA/REPERFUSION INJURY IN THE RAT1

2000 ◽  
Vol 69 (12) ◽  
pp. 2530-2537 ◽  
Author(s):  
Masamichi Katori ◽  
Tohru Tamaki ◽  
Tsuyoshi Takahashi ◽  
Mitsuko Tanaka ◽  
Akio Kawamura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Nitric Oxide Donor ◽  
Shock Proteins

scholarly journals A hősokkfehérjék hatása a máj ischaemiás-reperfúziós károsodására

2016 ◽  
Vol 157 (42) ◽  
pp. 1659-1666
Author(s):  
Andrea Rostás ◽  
Ahmed Sabry ◽  
Subhamay Ghosh
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Diseases ◽  
Diagnostic Role ◽  
Hepatic Ischemia Reperfusion ◽  
Shock Proteins

Hepatic ischemia-reperfusion injury as a result of inflow obstruction is a major cause of morbidity and mortality associated with liver pathologies and surgery. Heat shock proteins, a family of stress-inducible proteins involved in maintaining cell homeostasis and regulating the immune system play a major role in liver regeneration. They serve as crucial indicators of ischemia-reperfusion injury in human liver and influence liver function and recovery. The primary objectives of this article are to review the potential role of heat shock proteins as a diagnostic marker for liver diseases and therapeutic target in critical illness. The review will start by focusing on the essentials of heat shock proteins as an endogenous system as it relates to hepatic injury. It will elucidate the influence of heat shock protein-70 on hepatic diseases and ischemia-reperfusion. It will then look at their potential diagnostic role and finally highlights its activities as a possible therapeutic tool. Orv. Hetil., 2016, 157(42), 1659–1666.

HEAT SHOCK PROTEINS (HSPs): BIOMARKERS OF ISCHEMIA/REPERFUSION INJURY?

Shock ◽  
2002 ◽  
Vol 18 (Supplement) ◽  
pp. 9
Author(s):  
M C. Guisasola ◽  
M A. Peñaranda ◽  
L. López-Bescós ◽  
F. Asensio ◽  
A. Suárez ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Shock Proteins

Protective role of TAT-HSP70 after myocardial I/R injury

2017 ◽  
Vol 5 (3) ◽  
pp. 279-284
Author(s):  
Martin A. Meenakshi ◽  
Erik G. Seth
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Inflammatory Mechanism ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Shock Proteins

Myocardial ischemia reperfusion injury I/R adversely affects cardiac function. Heat shock proteins (HSPs) are a highly conserved family of proteins with diverse functions expressed by all cells exposed to environmental stress including myocardila injury. We investigated release of small constitutive heat shock proteins (HSPs) from mouse myocardium and the effects of TAT-HSP70 after myocardial I/R via occluding the left coronary artery (LAD). The results support the hypothesis that elevated HSPs in myocardium after ischemia and reperfusion and contributes to the inflammatory mechanism of myocardial functional injury. Further investigation of the significance of HSPs accumulation to the evolution of myocardial injury.

The 1990 Merck Frosst Award. Ischemic and reperfusion injury in the heart. Cellular mechanisms and pharmacological interventions

1991 ◽  
Vol 69 (6) ◽  
pp. 719-730 ◽  
Author(s):  
Morris Karmazyn
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Mitochondrial Function ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Prostaglandin Synthesis ◽  
Subsarcolemmal Mitochondria ◽  
Shock Proteins ◽  
Reperfused Myocardium

Reperfusion in the heart represents an important form of tissue injury, particularly in view of the emerging importance of reperfusion protocols aimed at salvaging the ischemic myocardium. Both the manifestations and the causes of reperfusion injury are multifold. With respect to the former, reperfusion injury can be characterized by various abnormalities including development of arrhythmias, contractile dysfunction, ultrastructural damage as well as various defects in intracellular biochemical homeostasis. The mechanisms underlying myocardial reperfusion injury are equally complex, but most likely involve numerous processes acting in concert resulting in eventual cell death. In this review, a description of various such potential mechanisms, which represent primary interests of the author, are presented. An understanding of these mechanisms has led to novel pharmacological approaches towards the protection of the reperfused myocardium. For instance, several lines of evidence implicate enhanced eicosanoid, and in particular prostaglandin, synthesis in reperfusion injury, since (1) such injury is involved with enhanced prostaglandin biosynthesis, (2) inhibition of prostaglandin synthesis with various nonsteroidal anti-inflammatory drugs attenuates injury, and (3) exogenous prostaglandins increase injury. Another intracellular process that is emerging as an important contributor to reperfusion injury in the heart is the Na+/H+ exchanger, which is most likely activated upon reperfusion. Such activation would lead to numerous intracellular disturbances including the increased synthesis of prostaglandins and elevated intracellular Ca2+ concentrations. Indeed, inhibitors of Na+/H+ exchange such as amiloride have been shown to effectively inhibit reperfusion injury. Reperfusion is also associated with depressed mitochondrial function, particularly in subsarcolemmal mitochondria which are rapidly injured as a result of both ischemic and reperfusion conditions. Preservation of mitochondrial function with dissimilar approaches such as carnitine or phosphatidylcholine administration markedly reduces reperfusion injury. A nonpharmacological novel approach towards the protection of the reperfused myocardium represents the induction of so-called stress or heart shock proteins in the heart prior to initiation of ischemia and reperfusion. The salutary effect of the heat shock response may be dependent not on the heat shock proteins themselves, but through the concomitant elevation of tissue catalase content resulting in enhanced detoxification of intracellular hydrogen peroxide. Thus reperfusion injury represents numerous complex events such that manipulations aimed at limiting such injury can be initiated to prevent specific defects with the ultimate goal of an overall reduction in cell damage.Key words: heart, ischemia, reperfusion, prostaglandins, leukotrienes, Na+/H+ exchange, subsarcolemmal mitochondria, interfibrillar mitochondria, heat shock proteins, tissue protection.

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