Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Osteoclasts in Bone Remodeling

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...

Bone Remodeling

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.

Hormones and Bone Tissue

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...

TGF - β Signaling Pathway

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...

Skeleton and Calcium Homeostasis

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

You might also read

Related Articles

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

Sort by

Same author

CCL20/CCR6 signaling modulates disease severity during the establishment of <i>Staphylococcus aureus</i> osteomyelitis.

mBio·2025

Same author

High-dose vitamin D to attenuate bone loss in patients with prostate cancer on androgen deprivation therapy: A phase 2 RCT.

Cancer·2024

Same author

Targeting Synovial Lymphatic Function as a Novel Therapeutic Intervention for Age-Related Osteoarthritis in Mice.

Arthritis & rheumatology (Hoboken, N.J.)·2023

Same author

Whole-genome RNA sequencing identifies distinct transcriptomic profiles in impingement cartilage between patients with femoroacetabular impingement and hip osteoarthritis.

Journal of orthopaedic research : official publication of the Orthopaedic Research Society·2022

Same author

Transcriptional regulation of cyclophilin D by BMP/Smad signaling and its role in osteogenic differentiation.

eLife·2022

Same author

IKKβ-NF-κB signaling in adult chondrocytes promotes the onset of age-related osteoarthritis in mice.

Science signaling·2021

Search research articles

Related Experiment Video

Updated: May 23, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

TRIP-1: a regulator of osteoblast function.

Diana Metz-Estrella¹, Jennifer H Jonason, Tzong-Jen Sheu

¹Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research

|March 31, 2012

Summary

Transforming growth factor β receptor interacting protein-1 (TRIP-1) is crucial for osteoblast differentiation and bone remodeling. Knocking down TRIP-1 inhibits osteoblast function and TGFβ signaling.

More Related Videos

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Related Experiment Videos

Last Updated: May 23, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

Bone biology
Cellular signaling
Molecular biology

Background:

Transforming growth factor β (TGFβ) receptor interacting protein-1 (TRIP-1) is expressed in osteoblasts.
TRIP-1 has a high affinity for tartrate-resistant acid phosphatase (TRAP).
TRIP-1 is suggested to positively regulate TGFβ signaling and osteoblast differentiation.

Purpose of the Study:

To characterize the role of TRIP-1 in osteoblast differentiation and bone remodeling.
To investigate the effect of various hormones and factors on TRIP-1 expression.
To determine the impact of TRIP-1 on TGFβ signaling pathways.

Main Methods:

TRIP-1 expression analysis in osteoblasts in vivo and in vitro.
Hormonal and factor treatment of primary osteoblasts.
Small interfering RNA (siRNA) mediated knockdown of TRIP-1.
Assessment of osteoblast differentiation markers (alkaline phosphatase, collagen I, Runx2, osteopontin, osteocalcin).
Cell cycle analysis and apoptosis assays.
TGFβ luciferase reporter assay.

Main Results:

TRIP-1 expression is dynamic during osteoblast differentiation, peaking at early stages.
Dexamethasone decreased TRIP-1, while vitamin D3, DHT, TGFβ1, and BMP-2 increased it.
TRIP-1 knockdown inhibited osteoblast differentiation, proliferation, and TGFβ signaling.
TRIP-1 knockdown caused cell cycle arrest in G2/M phase but did not induce apoptosis.

Conclusions:

TRIP-1 is abundant in osteoblasts and plays a critical role in early osteoblast maturation.
TRIP-1 expression is modulated by hormones and growth factors involved in bone remodeling.
TRIP-1 acts as a key positive regulator of osteoblast function by promoting differentiation, proliferation, and TGFβ signaling.