Related Experiment Video

Updated: Jul 23, 2025

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
09:32

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

8.8K

Icariin Promotes Osteogenic Differentiation in a Cell Model with NF1 Gene Knockout by Activating the cAMP/PKA/CREB

Meng Chen1,2,3, Lianhua Lu1, Dong Cheng1

  • 1Shandong Center for Disease Control and Prevention, Jinan 250014, China.

Molecules (Basel, Switzerland)
|July 14, 2023
PubMed

Insights

Icariin promotes bone growth in Neurofibromatosis type 1 (NF1) by activating the cAMP/PKA/CREB pathway. This study introduces a new therapeutic strategy for NF1-related bone defects.

Area of Science:

  • Genetics
  • Molecular Biology
  • Biochemistry

Background:

  • Neurofibromatosis type 1 (NF1) is a genetic disorder affecting bone development in up to 50% of patients.
  • The exact causes of bone issues in NF1 are unknown, with limited treatment options.

Purpose of the Study:

  • To investigate the molecular mechanisms behind NF1 bone disease.
  • To explore icariin's potential therapeutic effects on NF1-related bone defects.

Main Methods:

  • Created an osteoblast cell model with NF1 gene knockout.
  • Administered icariin to the NF1 cell model and analyzed its effects on the cAMP/PKA/CREB pathway.
  • Utilized a PKA inhibitor (H89) to confirm pathway involvement.

Main Results:

  • NF1 gene knockout decreased cAMP levels and osteogenic differentiation.
  • Icariin increased intracellular cAMP levels, activating the cAMP/PKA/CREB pathway.
  • Icariin significantly promoted osteoblast differentiation in the NF1 cell model, an effect blunted by H89.

Conclusions:

  • Icariin effectively promotes osteogenic differentiation in an NF1 cell model via the cAMP/PKA/CREB pathway.
  • This research provides a novel therapeutic approach for NF1 bone disease.
  • Findings pave the way for future drug development and clinical strategies for NF1 bone complications.
Keywords:
Neurofibromatosis type 1cAMP/PKA/CREBgene knockouticariinosteogenic differentiation

More Related Videos

Initiating Differentiation in Immortalized Multipotent Otic Progenitor Cells12:17

Initiating Differentiation in Immortalized Multipotent Otic Progenitor Cells

Published on: January 2, 2016

8.6K
Stimulation of Notch Signaling in Mouse Osteoclast Precursors08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

7.9K

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.5K
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...
3.7K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.4K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
4.2K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.7K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.6K