Related Experiment Video

Updated: Jul 22, 2026

Visualization of MG53-mediated Cell Membrane Repair Using in vivo and in vitro Systems
10:19

Visualization of MG53-mediated Cell Membrane Repair Using in vivo and in vitro Systems

Published on: June 30, 2011

Microfilament disruption occurs very early in ischemic proximal tubule cell injury

P S Kellerman1, R T Bogusky

  • 1Department of Internal Medicine, University of California, Davis, Sacramento.

Kidney International
|October 1, 1992
PubMed

Insights

Ischemic acute renal failure rapidly disrupts kidney proximal tubule microfilaments. This study shows significant filamentous actin loss within five minutes of ischemia, impacting kidney function.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pathophysiology

Background:

  • Ischemic acute renal failure damages proximal tubule apical membranes.
  • Previous studies indicated disruption of the proximal tubule apical cytoskeleton during ischemic injury using anti-actin antibodies.

Purpose of the Study:

  • To investigate the effect of ischemia on proximal tubule apical microfilaments using rhodamine-phalloidin.
  • To quantify the progressive disruption of filamentous actin (F-actin) in proximal tubules following ischemic injury.

Main Methods:

  • Utilized rhodamine-phalloidin staining, which specifically targets filamentous actin.
  • Applied graded durations of ischemia to experimental models.
  • Employed spectrofluorometry for quantitative analysis of F-actin levels.

Main Results:

  • Progressive disruption of proximal tubule apical microfilaments was observed with increasing ischemia duration.
  • 5, 15, and 50 minutes of ischemia led to significant decreases in apical F-actin (32.8%, 48.8%, and 58.4%, respectively).
  • No qualitative changes in glomerular or distal tubule F-actin structure were noted, although glomerular fluorescence increased non-progressively.

Conclusions:

  • Rhodamine-phalloidin is effective for qualitative and quantitative assessment of proximal tubule microfilaments in vivo.
  • Ischemia causes very early loss of proximal tubule apical microfilaments.
  • The majority of F-actin loss occurs within the first five minutes of ischemic insult.

More Related Videos

Imaging and Analysis of Neurofilament Transport in Excised Mouse Tibial Nerve09:52

Imaging and Analysis of Neurofilament Transport in Excised Mouse Tibial Nerve

Published on: August 31, 2020

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

Related Concept Videos

Actin Filament Depolymerization01:19

Actin Filament Depolymerization

Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
In F-actin, the ADF/cofilin proteins...
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
Microtubule Instability02:17

Microtubule Instability

Microtubules are hollow cylindrical filaments having a diameter of approximately 25 nm and a length that varies from 200 nm to 25 μm. GTP-bound tubulin subunits form αβ-heterodimers for microtubule assembly. These core building blocks interact longitudinally, polymerizing into protofilaments. The protofilaments then interact with one another through lateral bonding forces to form stable cylindrical microtubules. These cylindrical filaments are dynamic as they undergo repeated assembly and...
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
Cell Motility through Blebbing01:16

Cell Motility through Blebbing

Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
Blebbing Through the Matrix
In multicellular...
Disassembly of Intermediate Filaments01:35

Disassembly of Intermediate Filaments

Intermediate filaments (IFs) do not undergo spontaneous disassembly. Enzymes, kinases, and phosphatases add and remove phosphates from specific sites to regulate their disassembly. The IF concentration in the cytoplasm also regulates the disassembly. If the concentration crosses a threshold, it activates the protein kinases in the vicinity, allowing the phosphorylation of IFs.
Keratin proteins, found at the cell periphery near cell junctions, undergo a cycle of assembly and disassembly. In Type...