Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Genotypic variation in lead (Pb) accumulation dataset in sweetpotato flesh for 10 accessions from the United States of America.

Data in brief·2026
Same author

Genome-Wide Association Study of Sweet Potato Storage Root Traits Using GWASpoly, a Gene Dosage-Sensitive Model.

International journal of molecular sciences·2024
Same author

MYC is Sufficient to Generate Mid-Life High-Grade Serous Ovarian and Uterine Serous Carcinomas in a p53-R270H Mouse Model.

Cancer research communications·2024
Same author

MYC is sufficient to generate mid-life high-grade serous ovarian and uterine serous carcinomas in a p53-R270H mouse model.

bioRxiv : the preprint server for biology·2024
Same author

Autophagy modulating therapeutics inhibit ovarian cancer colony generation by polyploid giant cancer cells (PGCCs).

BMC cancer·2022
Same author

SWAN pathway-network identification of common aneuploidy-based oncogenic drivers.

Nucleic acids research·2022

Related Experiment Video

Updated: Jul 16, 2026

Expansion and Adipogenesis Induction of Adipocyte Progenitors from Perivascular Adipose Tissue Isolated by Magnetic Activated Cell Sorting
08:28

Expansion and Adipogenesis Induction of Adipocyte Progenitors from Perivascular Adipose Tissue Isolated by Magnetic Activated Cell Sorting

Published on: June 30, 2017

A role for bone morphogenetic protein-4 in adipocyte development.

Robert R Bowers1, M Daniel Lane

  • 1Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. rbowers4@jhmi.edu

Cell Cycle (Georgetown, Tex.)
|February 23, 2007
PubMed
Summary

Bone morphogenetic protein-4 (BMP-4) is crucial for initiating adipogenesis, the process of fat cell formation. This study reveals BMP-4

More Related Videos

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Rapid Isolation of BMPR-IB+ Adipose-Derived Stromal Cells for Use in a Calvarial Defect Healing Model
09:07

Rapid Isolation of BMPR-IB+ Adipose-Derived Stromal Cells for Use in a Calvarial Defect Healing Model

Published on: February 24, 2017

Related Experiment Videos

Last Updated: Jul 16, 2026

Expansion and Adipogenesis Induction of Adipocyte Progenitors from Perivascular Adipose Tissue Isolated by Magnetic Activated Cell Sorting
08:28

Expansion and Adipogenesis Induction of Adipocyte Progenitors from Perivascular Adipose Tissue Isolated by Magnetic Activated Cell Sorting

Published on: June 30, 2017

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Rapid Isolation of BMPR-IB+ Adipose-Derived Stromal Cells for Use in a Calvarial Defect Healing Model
09:07

Rapid Isolation of BMPR-IB+ Adipose-Derived Stromal Cells for Use in a Calvarial Defect Healing Model

Published on: February 24, 2017

Area of Science:

  • Cell Biology
  • Biochemistry
  • Developmental Biology

Background:

  • Obesity involves increased mature adipocyte numbers, originating from mesenchymal stem cells (MSCs).
  • The early commitment of MSCs to the adipocyte lineage remains poorly understood.
  • While later differentiation is well-studied, initial MSC commitment is a knowledge gap.

Purpose of the Study:

  • To investigate the role of bone morphogenetic protein-4 (BMP-4) in the earliest stages of adipogenesis.
  • To elucidate the mechanisms underlying mesenchymal stem cell commitment to the adipocyte lineage.
  • To explore the function of BMP-4 signaling in adipogenesis initiation.

Main Methods:

  • Treatment of growth-arrested 10T1/2 cells with BMP-4 to assess adipogenic response.
  • Analysis of BMP-4 expression in a preadipocyte cell line (A33) derived from 10T1/2 cells.
  • Investigating the necessity of endogenous BMP-4 for preadipocyte phenotype acquisition.

Main Results:

  • BMP-4 treatment enabled growth-arrested 10T1/2 cells to differentiate into adipocytes in response to hormonal stimuli.
  • A33 cells, which express BMP-4, demonstrated that endogenous BMP-4 is required for their preadipocyte characteristics.
  • These findings implicate BMP-4 in the critical commitment step of adipogenesis.

Conclusions:

  • Bone morphogenetic protein-4 (BMP-4) plays a key role in the commitment of mesenchymal stem cells to the adipocyte lineage.
  • BMP-4 signaling is essential for initiating adipogenesis, particularly the transition from MSCs to preadipocytes.
  • Further research into the BMP-4 pathway could offer new insights into obesity and metabolic disorders.