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Related Concept Videos

Autocrine Signaling01:01

Autocrine Signaling

Autocrine signaling is one of the many signaling mechanisms that function inside multicellular organisms to carry out intercellular communication. In this type of signaling mechanism, the same cell that secretes an extracellular signaling molecule also expresses the receptors to bind and respond to that signaling molecule.
Autocrine Signaling in Macrophages
Under normal physiological conditions, autocrine signaling is essential for maintaining homeostasis. This process is well characterized in...
Autocrine Signaling01:01

Autocrine Signaling

Autocrine signaling is one of the many signaling mechanisms that function inside multicellular organisms to carry out intercellular communication. In this type of signaling mechanism, the same cell that secretes an extracellular signaling molecule also expresses the receptors to bind and respond to that signaling molecule.
Autocrine Signaling in Macrophages
Under normal physiological conditions, autocrine signaling is essential for maintaining homeostasis. This process is well characterized in...
Hypothalamic-Pituitary Axis01:37

Hypothalamic-Pituitary Axis

The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Physiological Foundation of Stress01:24

Physiological Foundation of Stress

Stress triggers a coordinated physiological response involving the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis. This dual activation ensures that the body is prepared for both immediate and prolonged stress management. The process begins with the perception of a stressor. This initial phase activates the SNS, leading to the rapid release of adrenaline (epinephrine) from the adrenal glands.
Role of the Sympathetic Nervous System
Adrenaline triggers the...

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Related Experiment Video

Updated: Jul 18, 2026

Measurements of Physiological Stress Responses in C. Elegans
10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

Activated stress response pathways within multicellular aggregates utilize an autocrine component.

Graham D Jack1, M Carla Cabrera, Michael L Manning

  • 1Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA.

Cellular Signalling
|November 28, 2006
PubMed
Summary

Multicellular aggregates use autocrine cytokine signaling to survive metabolic arrest. This involves the Gadd45alpha/p38 pathway and AP-1 transcription factors, with responses varying by cell type and transformation state.

Related Experiment Videos

Last Updated: Jul 18, 2026

Measurements of Physiological Stress Responses in C. Elegans
10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

Area of Science:

  • Cell Biology
  • Signal Transduction
  • Cancer Research

Background:

  • Multicellular aggregates (spheroids) exhibit unique biological behaviors not seen in 2D cultures.
  • Understanding cellular responses to metabolic arrest is crucial for various biological contexts, including wound healing and tumor growth.

Purpose of the Study:

  • To investigate the signal transduction pathways involved in metabolic arrest and recovery in multicellular aggregates.
  • To compare the responses of normal fibroblasts (HFF-2) and glioblastoma cells (T98G) to metabolic arrest.

Main Methods:

  • Culturing primary human foreskin fibroblasts (HFF-2) and glioblastoma T98G cells as multicellular spheroids.
  • Inducing and monitoring long-term metabolic arrest (2 weeks) and subsequent recovery.
  • Analyzing cytokine production (IFN-gamma), pathway activation (Gadd45alpha/p38, AP-1), and transcription factor levels (c-jun, ATF3).
  • Investigating the role of NF-kappaB and JNK signaling in aggregate survival during arrest.

Main Results:

  • Spheroids entered and exited metabolic arrest via an autocrine response involving cytokine production (IFN-gamma).
  • The Gadd45alpha/p38 pathway and AP-1 transcription factors were activated, augmenting cytokine production.
  • HFF-2 aggregates survived arrest and recovered with NF-kappaB inhibition, independent of JNK, while T98G aggregates did not.
  • Cell type and transformation state influenced responses, highlighting the need for spheroid-based studies.

Conclusions:

  • Autocrine cytokine signaling is a key mechanism for spheroid survival during metabolic arrest.
  • The AP-1 transcription factor level is a convergence point for intracellular signaling in response to extracellular cues like spheroid formation and arrest.
  • Spheroid culturing provides insights into biological processes like wound healing and avascular tumor growth that are missed in monolayer cultures.