Related Experiment Video

Updated: Aug 9, 2026

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
04:33

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions

Published on: March 12, 2019

cfos and cjun antisense oligonucleotides block mitogenesis triggered by fibroblast growth factor-2 and ACTH in mouse

C F Lotfi1, H A Armelin

  • 1Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Brazil.

The Journal of Endocrinology
|March 10, 2001
PubMed

Insights

Fibroblast growth factor-2 (FGF2) and ACTH stimulate DNA synthesis in Y1 adrenal cells by inducing cFos and cJun proteins. Inhibiting these proteins blocks the stimulation, indicating a common pathway for cell growth.

Area of Science:

  • Cell biology
  • Molecular endocrinology
  • Adrenocortical cell function

Background:

  • Fibroblast growth factor-2 (FGF2) and adrenocorticotropic hormone (ACTH) are key regulators of cell growth.
  • The precise molecular mechanisms by which FGF2 and ACTH stimulate DNA synthesis in adrenocortical cells are not fully elucidated.
  • Understanding these pathways is crucial for comprehending adrenal gland development and function.

Purpose of the Study:

  • To investigate the role of cFos and cJun proteins in FGF2 and ACTH-induced DNA synthesis in Y1 adrenocortical cells.
  • To determine if FGF2 and ACTH signaling pathways converge on the induction of immediate early genes.
  • To elucidate the molecular basis of cell cycle re-entry in response to growth factors and hormones.

Main Methods:

  • Utilized G(0)/G(1) cell cycle-arrested mouse Y1 adrenocortical cells.
  • Administered short pulses of FGF2, synthetic ACTH(39), and natural porcine corticotropin A.
  • Quantified cFos and cJun protein induction using specific antibodies and antisense oligodeoxynucleotides (ODNs).
  • Assessed DNA synthesis stimulation via bromodeoxyuridine labeling index.

Main Results:

  • FGF2 induced cFos protein and stimulated DNA synthesis in a dose- and time-dependent manner, with a strong linear correlation between cFos induction and DNA synthesis.
  • ACTH also induced cFos protein and DNA synthesis, but the dose-response curves were not correlated.
  • Inhibition of cFos and cJun induction using antisense ODNs blocked DNA synthesis stimulation by both FGF2 and ACTH.
  • FGF2 and ACTH signaling pathways converge on the induction of cfos and cjun genes.

Conclusions:

  • FGF2 and ACTH signaling pathways converge at the level of cFos and cJun gene induction to trigger DNA synthesis in Y1 adrenocortical cells.
  • cFos and cJun proteins are essential mediators of FGF2 and ACTH-induced cell proliferation.
  • This study provides insights into the molecular mechanisms controlling cell cycle progression in the adrenal cortex.

More Related Videos

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

Establishment of Zone-Enriched Primary Cultures from the Mouse Adrenal Cortex07:43

Establishment of Zone-Enriched Primary Cultures from the Mouse Adrenal Cortex

Published on: May 8, 2026

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...