Related Experiment Video

Updated: Jun 25, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Reduced colonic apoptosis in mice overexpressing bovine growth hormone occurs through changes in several kinase

Fausto Bogazzi1, Federica Ultimieri, Francesco Raggi

  • 1Department of Endocrinology and Metabolism, University of Pisa, Ospedale Cisanello, Pisa, Italy. f.bogazzi@endoc.med.unipi.it

Growth Hormone & IGF Research : Official Journal of the Growth Hormone Research Society and the International IGF Research Society
|February 24, 2009
PubMed
Abstract

Insights

Growth hormone (GH) reduces colon cell death by decreasing pro-apoptotic proteins and increasing anti-apoptotic proteins. This protective effect in transgenic mice was reversed by blocking the GH receptor.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Gastroenterology

Background:

  • Growth hormone (GH) exhibits antiapoptotic properties in various cell types.
  • Acromegaly patients show reduced colonic mucosal apoptosis.
  • GH may play a role in colon cell apoptosis regulation.

Purpose of the Study:

  • Investigate the impact of GH on colonic apoptosis in transgenic mice.
  • Elucidate the molecular mechanisms underlying GH-mediated apoptosis regulation in the colon.
  • Assess the role of GH in protecting against apoptosis-inducing agents.

Main Methods:

  • TUNEL and Annexin V assays to quantify apoptosis in colonic epithelial cells.
  • Western blot analysis to assess pro- and anti-apoptotic protein expression.
  • Inhibition of GH action using a selective GH receptor antagonist.

Main Results:

  • Transgenic mice overexpressing GH (Acro) exhibited significantly lower colonic apoptosis compared to controls.
  • GH-mediated antiapoptotic effects involve modulation of key proteins (e.g., Bcl-2, Bax, Bad) and caspase activation.
  • Treatment with a GH receptor antagonist reversed the antiapoptotic phenotype, confirming a direct GH effect.
  • The antiapoptotic colonic phenotype in Acro mice conferred protection against doxorubicin-induced apoptosis.

Conclusions:

  • GH significantly reduces colonic apoptosis in both young and elder transgenic animals.
  • This effect is mediated by shifting the balance towards anti-apoptotic proteins via kinase pathways (p38, p44/42, PI3K).
  • GH receptor antagonism abolishes the antiapoptotic effects, highlighting the direct role of GH signaling.

More Related Videos

Ileectomy-induced Bile Overaccumulation in Mouse Intestine06:55

Ileectomy-induced Bile Overaccumulation in Mouse Intestine

Published on: August 21, 2017

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
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...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...