Growth Factor Withdrawal
Growth Factor Withdrawal - Related Videos
11:51
Blood Withdrawal I
0 Views •
2016
Source: Kay Stewart, RVT, RLATG, CMAR; Valerie A. Schroeder, RVT, RLATG. University of Notre Dame, IN Blood collection is a common requirement for research studies that involve mice and rats. The method of blood withdrawal in mice and rats is dependent upon the volume of blood needed, the frequency of the sampling, the health status of the animal to be bled, and the skill level of the technician. All methods discussed-retro-orbital sinus bleeds, initial tail snip bleeds, and intracardiac...
06:32
Blood Withdrawal II
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2016
Source: Kay Stewart, RVT, RLATG, CMAR; Valerie A. Schroeder, RVT, RLATG. University of Notre Dame, IN The collection of blood from mice and rats for analysis can be done through a variety of methods. Each method of collection has variations in the type of restraint required, the invasiveness of the procedure, and the necessity of a general anesthetic.1Historically, the use of the retro-orbital sinus cavity has been used, but not without debate. The controversy related to the potential tissue...
18:27
Preparing T Cell Growth Factor from Rat Splenocytes
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Cited by 12 •
2007
We describe the preparation of T cell growth factor used for the in vitro expansion of antigen-specific rat T lymphocyte lines.
09:04
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
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Cited by 7 •
2016
We describe a simple cell-based bioassay for detecting, quantifying and monitoring the activity of members of the vascular endothelial growth factor family of ligands. The assay uses chimeric receptors expressed in a factor-dependent cell line to provide a semi-quantitative or quantitative assessment of receptor binding and cross-linking by the ligand.
09:29
Electrospinning Growth Factor Releasing Microspheres into Fibrous Scaffolds
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Cited by 10 •
2014
This protocol combines electrospinning and microspheres to develop tissue engineered scaffolds to direct neurons. Nerve growth factor was encapsulated within PLGA microspheres and electrospun into Hyaluronic Acid (HA) fibrous scaffolds. The protein bioactivity was tested by seeding the scaffolds with primary chick Dorsal Root Ganglia and culturing for 4-6 days.
FAQs
Removing a trophic ligand lowers survival-promoting signaling through PI3K-AKT, weakening pathways that normally support neuronal viability. This loss can engage mitochondrial apoptosis, a regulated death pathway in which cytochrome c is released and caspases become activated. Tracking these linked events helps connect extracellular signal loss with the intracellular execution of neuronal death.
The response reveals trophic dependence: neurons that require nerve growth factor or related ligands become vulnerable when those signals disappear. In developmental neuroscience, this condition helps identify how strongly neuronal populations rely on extracellular support. Comparing responses across systems can clarify survival requirements and separate dependence on trophic signaling from later mechanisms that execute cell death.
Cytochrome c release and caspase activation indicate that loss of survival signaling has progressed toward mitochondrial apoptosis rather than representing only a change in receptor signaling. Their appearance links the upstream reduction in PI3K-AKT activity to a defined cell-death pathway. These events therefore help researchers map where neuronal survival responses give way to irreversible damage.
A basic design compares neuronal systems receiving their usual nerve growth factor or related ligand with systems from which that support is removed. Researchers can then examine changes in PI3K-AKT signaling, mitochondrial apoptosis, cytochrome c release, caspase activation, and neuronal viability. This paired comparison isolates the consequences of losing extracellular survival signals.
Measurements can show whether neurons primarily lose pro-survival signaling, activate mitochondrial apoptosis, or proceed to reduced viability after support is removed. Examining PI3K-AKT activity alongside cytochrome c release and caspase activation provides a mechanistic sequence rather than a single endpoint. The resulting profile helps evaluate how neuronal cells respond to trophic stress.
The model recreates a controlled loss of neuronal support, allowing researchers to study mechanisms that may contribute to neurodegenerative damage. It also provides a setting for testing neuroprotective responses aimed at preserving neuronal viability. Because the system links trophic signaling, mitochondrial apoptosis, and cell survival, it can connect basic neuroscience with strategies for limiting neuronal loss.