Repair and Regeneration of the Wounded Cell Membrane

Poellmann, Michael J.; Lee, Raphael C.

doi:10.1007/s40883-017-0031-1

Cited by 11 publications

(18 citation statements)

References 307 publications

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“…The triblock copolymer P188 has been shown to rescue a variety of tissues and cell types from I/R injury in different settings [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 36 , 37 , 38 ]. More recently, profound improvements in mitochondrial function through P188 after I/R injury have become apparent [ 9 , 10 , 11 , 12 , 18 , 39 , 40 ], suggesting possible direct interactions of P188 with mitochondria, specifically by stabilizing their membrane.…”

Section: Discussionmentioning

confidence: 99%

“…P188′s superb protective effects after I/R injury have been recreated in various experimental settings [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 36 , 37 , 38 ]. Therefore, injuring mitochondria in a way that mimics the patho-physiological processes of I/R in living cells was the premise to show any direct effects of P188 on mitochondria.…”

Section: Discussionmentioning

confidence: 99%

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Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro

Pille

Riess

2021

Brain Sciences

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Outcome after cerebral ischemia is often dismal. Reperfusion adds significantly to the ischemic injury itself. Therefore, new strategies targeting ischemia/reperfusion (I/R) injury are critically needed. Poloxamer (P)188, an amphiphilic triblock copolymer, is a highly promising pharmacological therapeutic as its capability to insert into injured cell membranes has been reported to protect against I/R injury in various models. Although mitochondrial function particularly profits from P188 treatment after I/R, it remains unclear if this beneficial effect occurs directly or indirectly. Here, rat isolated brain mitochondria underwent oxidative stress in vivo by asphyxial cardiac arrest or in vitro by the addition of hydrogen peroxide (H2O2) after isolation. Mitochondrial function was assessed by adenosine triphosphate synthesis, oxygen consumption, and calcium retention capacity. Both asphyxia and H2O2 exposure significantly impaired mitochondrial function. P188 did not preserve mitochondrial function after either injury mechanism. Further research is indicated.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro

Pille

Riess

2021

Brain Sciences

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“…It is likely our observations still hold in the presence of such effects as these temperatures must be sustained for minutes for observable damage to occur. 58 However, further investigations will be required to elucidate the quantitative relationship between membrane permeability and cell viability.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Cell Membrane Permeability In Vitro Part I: Transport Behavior Induced by Single-Pulse Electric Fields*

Sweeney

Weaver

Davalos

2018

Technol Cancer Res Treat

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Most experimental studies of electroporation focus on permeabilization of the outer cell membrane. Some experiments address delivery of ions and molecules into cells that should survive; others focus on efficient killing of the cells with minimal temperature rise. A basic method for quantifying electroporation effectiveness is measuring the membrane’s diffusive permeability. More specifically, comparisons of membrane permeability between electroporation protocols often rely on relative fluorescence measurements, which are not able to be directly connected to theoretical calculations and complicate comparisons between studies. Here we present part I of a 2-part study: a research method for quantitatively determining the membrane diffusive permeability for individual cells using fluorescence microscopy. We determine diffusive permeabilities of cell membranes to propidium for electric field pulses with durations of 1 to 1000 μs and strengths of 170 to 400 kV/m and show that diffusive permeabilities can reach 1.3±0.4×10−8 m/s. This leads to a correlation between increased membrane permeability and eventual propidium uptake. We also identify a subpopulation of cells that exhibit a delayed and significant propidium uptake for relatively small single pulses. Our results provide evidence that cells, especially those that uptake propidium more slowly, can achieve large permeabilities with a single electrical pulse that may be quantitatively measured using standard fluorescence microscopy equipment and techniques.

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“…P188 offered in vitro neuroprotection, amongst other, through cell viability increase, reduction in LDH release, apoptosis and necrosis, and improved morphological appearances after mechanically induced TBI with fluid shear stress [ 16 , 17 , 18 , 20 , 21 , 22 ]. Generally, P188 has been observed to seal membrane leakage, thus, preventing cell damage and death [ 8 , 23 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury

Meyer

Riess

2021

Life

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Traumatic brain injury (TBI) leads to morbidity and mortality worldwide. Reperfusion after ischemia adds detrimental injury to cells. Ischemia/reperfusion (I/R) injures cells in a variety of ways including cell membrane disruption. Hence, methods to improve endogenous membrane resealing capacity are crucial. Poloxamer (P) 188, an amphiphilic triblock copolymer, was found to be effective against I/R and mechanical injury in various experimental settings. The aim of this study was to establish an in vitro mouse neuronal TBI model and, further, to investigate if postconditioning with P188 directly interacts with neurons after compression and simulated I/R injury, when administered at the start of reoxygenation. Cellular function was assessed by cell number/viability, mitochondrial viability, membrane damage by lactated dehydrogenase (LDH) release and FM1-43 incorporation as well as apoptosis-activation by Caspase 3. Five hours hypoxia ± compression with 2 h reoxygenation proved to be a suitable model for TBI. Compared to normoxic cells not exposed to compression, cell number and mitochondrial viability decreased, whereas membrane injury by LDH release/FM1-43 dye incorporation and Caspase 3 activity increased in cells exposed to hypoxic conditions with compression followed by reoxygenation. P188 did not protect neurons from simulated I/R and/or compression injury. Future research is indicated.

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Repair and Regeneration of the Wounded Cell Membrane

Cited by 11 publications

References 307 publications

Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro

Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro

Characterization of Cell Membrane Permeability In Vitro Part I: Transport Behavior Induced by Single-Pulse Electric Fields*

Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury

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