Dead Cell Inhibition
Dead Cell Inhibition - Related Videos
10:47
Quantification of Proliferative and Dead Cells in Enteroids
0 Views •
Cited by 2 •
2020
The presented protocol uses flow cytometry to quantify the number of proliferating and dead cells in cultured mouse enteroids. This method is helpful to evaluate the effects of drug treatment on organoid proliferation and survival.
09:48
In vitro Quantitative Imaging Assay for Phagocytosis of Dead Neuroblastoma Cells by iPSC-Macrophages
0 Views •
Cited by 7 •
2021
Neurodegenerative diseases are associated with dysregulated microglia functions. This article outlines an in vitro assay of phagocytosis of neuroblastoma cells by iPSC-macrophages. Quantitative microscopy readouts are described for both live-cell time-lapse imaging and fixed-cell high-content imaging.
02:58
Immunoblot Analysis of Apoptosis Inhibition in Host Cells Expressing an Antiapoptotic Bacterial Protein
0 Views •
2026
Source: Berens, C. et al. Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling. J. Vis. Exp. (2015)This video demonstrates the use of immunoblotting to assess apoptosis inhibition by the bacterial effector protein CaeB in human cells. It outlines the steps for detecting apoptotic markers following doxycycline-induced expression of pro-apoptotic proteins in host cells expressing the effector.
08:38
Habituation and Prepulse Inhibition of Acoustic Startle in Rodents
0 Views •
Cited by 164 •
2011
Habituation and prepulse inhibition of startle are operational measures of sensory gating. Sensory gating is disrupted in schizophrenia, and some other mental disorders and neurodegenerative diseases. We here describe a standard protocol to assess short-term and long-term habituation as well as prepulse inhibition of acoustic startle responses in rats and mice.
03:44
siRNA-Based Inhibition of Autophagy in Herpes Simplex Virus-Infected Immature Dendritic Cells
0 Views •
2025
This video demonstrates a small interfering RNA (siRNA)-based technique to interfere with autophagic flux. A siRNA targeting FIP200 mRNA is introduced into monocyte-derived immature dendritic cells (iDCs) using electroporation, causing the knockdown of FIP200 expression and leading to the inhibition of nuclear lamin disruption via autophagy. Upon adding herpes simplex virus (HSV), the nuclear egress of viral progeny is inhibited due to the absence of lamin disruption via autophagic flux.
FAQs
Intracellular contents, damage-associated signals, and other soluble factors can alter the environment around living cells. These released materials may create stress, promote inflammation, or induce growth arrest in neighboring cells. Their effects help explain why nonviable cells can influence nearby tissue or cultured cells even when the living cells were not initially damaged.
The surrounding environment influences how strongly nearby living cells respond to dead-cell material. Changes caused by released contents or soluble factors may produce cellular stress, inflammatory responses, or reduced growth. Consequently, the same population of nonviable cells can have different consequences depending on how much dead material accumulates and how effectively it is cleared.
Accumulation increases the presence of dead cells and their remnants in a local area, potentially extending exposure of living cells to inhibitory signals. Clearance can limit that exposure and support recovery of the surrounding tissue or culture. Studying both processes helps researchers connect the presence of dead cells with inflammation, growth changes, and tissue outcomes.
Researchers can assess how nonviable cells or their remnants affect nearby living cells by monitoring changes in survival, growth, or activity. Comparing these responses with the presence or absence of dead-cell material helps reveal whether neighboring cells experience a secondary inhibitory effect. This approach also supports separation of direct cell death from responses caused by the local environment.
The analysis can help distinguish direct effects of cell death from secondary responses in surrounding cells. Reduced survival, altered growth, or decreased activity among nearby living cells may reflect exposure to released intracellular contents, damage-associated signals, or soluble factors rather than death of those cells themselves. This distinction improves interpretation of tissue and cell-culture experiments.
The phenomenon is relevant to tissue injury, infection, cancer biology, and regenerative research. In each setting, dead-cell accumulation and clearance can influence inflammation, recovery, or experimental outcomes. Considering these interactions helps researchers interpret how damaged or dying cells affect neighboring populations and how local cellular conditions may shape disease or repair processes.