scholarly journals 3, 4-dihydroxyl-phenyl lactic acid restores NADH dehydrogenase 1 α subunit 10 to ameliorate cardiac reperfusion injury

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Xiao-Yuan Yang ◽  
Ke He ◽  
Chun-Shui Pan ◽  
Quan Li ◽  
Yu-Ying Liu ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Reperfusion Injury ◽  
Nadh Dehydrogenase ◽  
Α Subunit

scholarly journals Deletion of the Gamma Subunit of ENaC in Endothelial Cells Does Not Protect against Renal Ischemia Reperfusion Injury

2021 ◽  
Vol 22 (20) ◽  
pp. 10914
Author(s):  
Stephanie M. Mutchler ◽  
Mahpara Hasan ◽  
Donald E. Kohan ◽  
Thomas R. Kleyman ◽  
Roderick J. Tan
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Α Subunit ◽  
Γ Subunit ◽  
Renal Ischemia Reperfusion Injury

Acute kidney injury due to renal ischemia-reperfusion injury (IRI) may lead to chronic or end stage kidney disease. A greater understanding of the cellular mechanisms underlying IRI are required to develop therapeutic options aimed at limiting or reversing damage from IRI. Prior work has shown that deletion of the α subunit of the epithelial Na+ channel (ENaC) in endothelial cells protects from IRI by increasing the availability of nitric oxide. While canonical ENaCs consist of an α, β, and γ subunit, there is evidence of non-canonical ENaC expression in endothelial cells involving the α subunit. We therefore tested whether the deletion of the γ subunit of ENaC also protects mice from IRI to differentiate between these channel configurations. Mice with endothelial-specific deletion of the γ subunit and control littermates were subjected to unilateral renal artery occlusion followed by 48 h of reperfusion. No significant difference was noted in injury between the two groups as assessed by serum creatinine and blood urea nitrogen, levels of specific kidney injury markers, and histological examination. While deletion of the γ subunit did not alter infiltration of immune cells or cytokine message, it was associated with an increase in levels of total and phosphorylated endothelial nitric oxide synthase (eNOS) in the injured kidneys. Our studies demonstrate that even though deletion of the γ subunit of ENaC may allow for greater activation of eNOS, this is not sufficient to prevent IRI, suggesting the protective effects of α subunit deletion may be due, in part, to other mechanisms.

Hypoxia and ischemia-reperfusion: a BiK contribution?

2014 ◽  
Vol 307 (6) ◽  
pp. H811-H817 ◽  
Author(s):  
Jean-Yves Tano ◽  
Maik Gollasch
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Calcium Influx ◽  
Ischemia Reperfusion ◽  
Ischemic Injury ◽  
Bk Channels ◽  
Bk Channel ◽  
Protective Function ◽  
Α Subunit ◽  
Excess Calcium

Over the last decades, cardiovascular disease has become the primary cause of death in the Western world, and this trend is expanding throughout the world. In particular, atherosclerosis and the subsequent vessel obliterations are the primary cause of ischemic disease (stroke and coronary heart disease). Excess calcium influx into the cells is one of the major pathophysiological mechanisms important for ischemic injury in the brain and heart in humans. The large-conductance calcium-activated K+ channels (BK) are thus interesting candidates to protect against excess calcium influx and the events leading to ischemic injury. Indeed, the mitochondrial BK channels (mitoBK) have recently been shown to play a protective function against ischemia-reperfusion injury both in vitro and in animal models, although the exact mechanism of this protection is still under scrutiny. In addition, in both the plasma membrane and mitochondrial BK channel, the α-subunit itself is sensitive to hypoxia. This sensitivity is tissue specific and conferred by a highly conserved motif within an alternatively spliced cysteine-rich insert (STREX) in the intracellular C terminus of the channel. This review describes recent developments of the increasing relevance of BK channels in hypoxia and ischemia-reperfusion injury.

Demonstration of Retinal Glycogen with Silver Methenamine

1971 ◽  
Vol 29 ◽  
pp. 564-565
Author(s):  
A. W. Sedar ◽  
G. H. Bresnick
Keyword(s):  
Lactic Acid ◽  
Chromic Acid ◽  
Periodic Acid ◽  
Müller Cell ◽  
External Limiting Membrane ◽  
Electron Microscope Level ◽  
Reactive Process ◽  
Inner Limiting Membrane ◽  
Muller Cell ◽  
And Migration

After experimetnal damage to the retina with a variety of procedures Müller cell hypertrophy and migration occurs. According to Kuwabara and others the reactive process in these injuries is evidenced by a marked increase in amount of glycogen in the Müller cells. These cells were considered originally supporting elements with fiber processes extending throughout the retina from inner limiting membrane to external limiting membrane, but are known now to have high lactic acid dehydrogenase activity and the ability to synthesize glycogen. Since the periodic acid-chromic acid-silver methenamine technique was shown to demonstrate glycogen at the electron microscope level, it was selected to react with glycogen in the fine processes of the Müller cell that ramify among the neural elements in various layers of the retina and demarcate these cells cytologically. The Rhesus monkey was chosen as an example of a well vascularized retina and the rabbit as an example of a avascular retina to explore the possibilities of the technique.

Factors affecting the ability of dental cements to alter the pH of lactic acid solutions

2000 ◽  
Vol 27 (12) ◽  
pp. 1030-1033 ◽  
Author(s):  
M. Patel ◽  
H. Tawfik ◽  
Y. Myint ◽  
D. Brocklehurst ◽  
J. W. Nicholson
Keyword(s):  
Lactic Acid ◽  
Acid Solutions ◽  
Factors Affecting

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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