Ameloblastin upstream region contains structural elements regulating transcriptional activity in a stromal cell line derived from bone marrow.

Ameloblastin (AMBN) was originally described as a tooth-specific extracellular matrix protein, but current data have shown that AMBN is present in many different tissues of mesenchymal origin. The identification of regulatory elements in the promoter region of the Ambn gene would assist in identifying potential mesenchymal-specific transcriptional factors. In this study we subcloned a 3,788-bp region upstream (and a 54-bp region downstream) of the mouse Ambn transcriptional start site into a LacZ reporter construct and called this construct 3788-Ambn-lacZ.

LBP and sCD14 patterns in total hip replacement surgery performed during combined spinal/epidural anaesthesia.

Background: Danger patterns and pattern recognition receptors have been targets in the investigation and treatment of systemic inflammatory response syndrome and sepsis. Lipopolysaccharide (LPS)-binding protein (LBP) presents LPS and gram-positive bacterial cell wall products to the receptors TLR4/MD-2 and TLR2, respectively. Low concentrations of LBP stimulate responses to LPS and peptidoglycan, whereas higher concentrations inhibit these responses.

Ameloblastin expression and putative autoregulation in mesenchymal cells suggest a role in early bone formation and repair.

Ameloblastin is mainly known as a dental enamel protein, synthesized and secreted into developing enamel matrix by the enamel-forming ameloblasts. The function of ameloblastin in tooth development remains unclear, but it has been suggested to be involved in processes varying from regulating crystal growth to activity as a growth factor or partaking in cell signaling. Recent studies suggest that some enamel matrix proteins also might have important functions outside enamel formation.

Ameloblastin promotes bone growth by enhancing proliferation of progenitor cells and by stimulating immunoregulators.

In this study, we examined the role of the enamel matrix protein, ameloblastin, in bone growth and remodelling, and attempted to identify some of the molecular mechanisms involved in these processes. The effects of recombinant ameloblastin (rAmbn) were tested in vivo in rats, and in vitro in primary human mesenchymal stem cells, osteoblasts, chondrocytes, and osteoclasts. We used a microarray technique to identify genes that were regulated in human osteoblasts and verified our findings using multiplex protein analysis and real-time RT-PCR.

Local and systemic chemokine patterns in a human musculoskeletal trauma model.

Objective And Design: This prospective study aims to identify differences in local and systemic chemokines kinetics within 24 h of a standardised human surgical trauma (total hip arthroplasty) and their impact on systemic polymorphonuclear cells.

Materials And Methods: We examined seven patients with coxarthrosis, but without comorbidity, who had a total hip arthroplasty. Local drained blood and systemic blood samples were collected at wound closure and at 1, 4, and 24 h after surgery.

Liver X receptor is a key regulator of cytokine release in human monocytes.

Aberrant regulation of innate immune responses and uncontrolled cytokine bursts are hallmarks of sepsis and endotoxemia. Activation of the nuclear liver X receptor (LXR) was recently demonstrated to suppress inflammatory genes. Our aim was to investigate the expression of LXR in human monocytes under normal and endotoxemic conditions and to study the influence of LXR activation on endotoxin-induced cytokine synthesis and release.

Expression and regulation of resistin in osteoblasts and osteoclasts indicate a role in bone metabolism.

The adipose tissue is the site of expression and secretion of a range of biologically active proteins, called adipokines, for example, leptin, adiponectin, and resistin. Leptin has previously been shown to be expressed in osteoblasts and to promote bone mineralization, whereas adiponectin expression is enhanced during osteoblast differentiation. In the present study we explored the possible role of resistin in bone metabolism.