Destruction of microfilament bundles in mouse embryo fibroblasts treated with inhibitors of energy metabolism

Bershadsky, Alexander D.; Gelfand, Vladimir I.; Svitkina, Tatyana; Tint, I.S.

doi:10.1016/0014-4827(80)90446-2

Cited by 103 publications

(37 citation statements)

References 22 publications

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“…2). Microfilament disruption during ischemia may be the result of cellular ATP depletion as metabolic inhibitors result in breakdown of actin microfilaments in cell culture studies (71). Taken together, these data indicate that the cell's inability to maintain surface membrane polarity may correlate with the disruption of lateral cell-cell attachments and the actin cytoskeleton.…”

Section: Altered Epithelial Cell Polarity In Pathologic Statesmentioning

confidence: 87%

Alterations in the establishment and maintenance of epithelial cell polarity as a basis for disease processes.

1990

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Section: Altered Epithelial Cell Polarity In Pathologic Statesmentioning

confidence: 87%

Alterations in the establishment and maintenance of epithelial cell polarity as a basis for disease processes.

1990

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“…Cells were fixed with 3.7% formaldehyde in SB and washed with PBS. This preparation method for immunostaining extracts soluble proteins and improves visualization of the cytoskeletal structures (22). After blocking nonspecific binding by preincubating cells with 3% BSA in PBS, the cells were incubated for 1 h with the anti-actin Ab (1 st Ab; Sigma), diluted 1:100 in blocking solution.…”

Section: Methodsmentioning

confidence: 99%

“…7). Positive control neurons that were treated with 1 mM hydrogen peroxide (22) were TUNELpositive (n ϭ 8), and cofilin(S3E)-GFP-expressing neurons (n ϭ 4) and buffer-injected control neurons (n ϭ 5) were TUNEL-negative. These data showed that nucleolytic apoptosis was not induced by cofilin overexpression, and the effects of cofilin overexpression on synaptic strength and plasticity are unlikely to be due to apoptotic processes.…”

Section: Synapse Loss By Cofilin-actin Rod Formation Is Not Caused Bymentioning

confidence: 99%

Cofilin expression induces cofilin-actin rod formation and disrupts synaptic structure and function in Aplysia synapses

Jang

Han

Lee

et al. 2005

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

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Cofilin-actin rods are inclusion-like structures that are induced by certain chemical or physical stresses in cultured cells, and the rods formed in neurons are thought to be associated with neurodegeneration. Here, we cloned an Aplysia cofilin homolog and overexpressed it in cultured neurons. Overexpressed cofilin formed rod-like structures that included actin. The overall neuronal morphology was unaffected by cofilin overexpression; however, a decrease in number of synaptic varicosities was observed. Consistent with this structural change by cofilin overexpression, the synaptic strength was reduced, and furthermore, the long-term facilitation elicited by repeated pulses of 5-hydroxytryptamine was impaired in sensory-to-motor synapses. However, cofilin overexpression did not induce programmed cell death. These findings suggest that the formation of cofilin-actin rod-like structures can lead to neurodegeneration, and this might be a mechanism of rundown of neuronal and synaptic function without cell death in neurodegenerative diseases.neurodegeneration ͉ Hirano body ͉ long-term facilitation

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“…Beef pancrease DNAase I (Sigma Immunochemicals) was mixed with 3 ml of calf thymus DNA type I (Sigma Immunochemicals) to obtain a maximal rate of0. 25 Whole rat kidneys were quickly frozen between stainless steel tongs cooled in liquid nitrogen and pulverized with a liquid nitrogen-cooled stainless steel mortar and pestle in preparation for extraction. After a small amount of the powdered tissue was placed in a drying oven at 105°C for 24 h, the remainder was placed in a centrifuge tube on crushed dry ice and extracted with cold 8% perchlorate (3.5:1 wt/wt).…”

Section: Methodsmentioning

confidence: 99%

Exogenous adenosine triphosphate (ATP) preserves proximal tubule microfilament structure and function in vivo in a maleic acid model of ATP depletion.

Kellerman¹

1993

J. Clin. Invest.

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The hallmark of ischemic acute renal failure is a rapid and early decline in proximal tubule ATP. Since we have previously shown that over half of apical microfilament losses occur within the first 5 min of experimental ischemic injury, we postulated that microfilament (F-actin) structure and cellular location are dependent on cellular ATP levels. To test this hypothesis, we used maleic acid to selectively inhibit renal cortical ATP production in vivo. Maleic acid significantly decreased tissue ATP and apical F-actin in a dose-dependent manner relative to equimolar sodium chloride controls, yet higher doses of maleic acid quantitatively resulted in net actin polymerization, primarily in the cytoplasm. Functionally, maleic acid decreased glomerular filtration rate (GFR) and tubular reabsorption of sodium (TRN.) in a dose-dependent manner relative to sodium chloride controls. Administration of exogenous ATP resulted in significant increases in tissue ATP, net actin depolymerization, and relocation of F-actin from the cytoplasm back to the apical surface coinciding with increases in GFR and TRN,. Thus, ATP depletion induced by maleic acid resulted in significant cytoskeletal and functional alterations that were ameliorated by exogenous ATP. We therefore conclude that the structure and cellular location of F-actin necessary for normal functioning of proximal tubule cells in vivo is dependent on tissue ATP levels. (J.

show abstract

Destruction of microfilament bundles in mouse embryo fibroblasts treated with inhibitors of energy metabolism

Cited by 103 publications

References 22 publications

Alterations in the establishment and maintenance of epithelial cell polarity as a basis for disease processes.

Alterations in the establishment and maintenance of epithelial cell polarity as a basis for disease processes.

Cofilin expression induces cofilin-actin rod formation and disrupts synaptic structure and function in Aplysia synapses

Exogenous adenosine triphosphate (ATP) preserves proximal tubule microfilament structure and function in vivo in a maleic acid model of ATP depletion.

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