The expression of monocyte chemoattractant protein-1 and other chemokines by osteoblasts

Graves, Dana T.

doi:10.2741/a453

Cited by 54 publications

(35 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accordingly, we selected six genes for real-time RT-PCR validation, which are CCR3 (chemokine (C-C motif) receptor 3), HDC (histidine decarboxylase), GCR (glucocorticoid receptor), RAMP3 (receptor (calcitonin) activity-modifying protein 3), SCYE1 (small inducible cytokine subfamily E, member 1), and FCER1A (Fc fragment of IgE, high affinity I, receptor for ␣-polypeptide). These genes and/or their products, through modulation of monocytes, are known to participate in bone monocyte recruitment (CCR3, HDC) (15,25), osteoclastogenesis (GCR, HDC, CCR3) (26 -31), osteoclast regulation (HDC, RAMP3) (32,33), and/or production of proinflammatory cytokines important to osteoporosis (SCYE1, FCER1A) (34,35).…”

Section: Degs Validated Through Real-time Rt-pcr-mentioning

confidence: 99%

“…Chemotaxis is a major mechanism whereby circulating monocytes migrate into the bone microenvironment (15). Given that CCR3 ligand, RANTES (Chemokine, CC motif, ligand 5), was found in both osteoblasts and osteoclasts (38 -40), CCR3 may play an important role in the recruitment of monocytes into bone.…”

Section: Degs Validated Through Real-time Rt-pcr-mentioning

confidence: 99%

“…Recruitment of circulating monocytes into bone is modulated mainly by chemotaxis (15), whereby monocyte chemoattractants from bone and their receptors on monocytes, such as chemokine receptors, interact to initiate and maintain a directed migration of monocytes toward bone tissue.…”

mentioning

confidence: 99%

See 2 more Smart Citations

A Novel Pathophysiological Mechanism for Osteoporosis Suggested by an in Vivo Gene Expression Study of Circulating Monocytes

Liu

Dvornyk

Lü

et al. 2005

Journal of Biological Chemistry

115

128

View full text Add to dashboard Cite

Bone mineral density (BMD) is a major risk factor for osteoporosis. Circulating monocytes may serve as early progenitors of osteoclasts and produce a wide variety of factors important to bone metabolism. However, little is known about the roles of circulating monocytes in relation to the pathophysiology of osteoporosis. Using the Affymetrix HG-U133A GeneChip® array, we performed a comparative gene expression study of circulating monocytes in subjects with high and low BMD. We identified in total 66 differentially expressed genes including some novel as well as some already known to be relevant to bone metabolism. Three genes potentially contributing to bone metabolism, CCR3 (chemokine receptor 3), HDC (histidine decarboxylase, i.e. the histamine synthesis enzyme), and GCR (glucocorticoid receptor), were confirmed by quantitative real-time reverse transcriptase-PCR as up-regulated in subjects with lower BMD. In addition, significant negative correlation was observed between expression levels of the genes and BMD Z-scores. These three genes and/or their products mediate monocyte chemotaxis, histamine production, and/or sensitivity to glucocorticoids. Our results suggest a novel pathophysiological mechanism for osteoporosis that is characterized by increased recruitment of circulating monocyte into bone, enhanced monocyte differentiation into osteoclasts, as well as osteoclast stimulation via monocyte functional changes. This is the first in vivo microarray study of osteoporosis in humans. The results may contribute to identification of new genes and their functions for osteoporosis and suggest genetic markers to discern individuals at higher risk to osteoporosis with an aim for preventive intervention and treatment.

show abstract

Section: Degs Validated Through Real-time Rt-pcr-mentioning

confidence: 99%

Section: Degs Validated Through Real-time Rt-pcr-mentioning

confidence: 99%

See 1 more Smart Citation

A Novel Pathophysiological Mechanism for Osteoporosis Suggested by an in Vivo Gene Expression Study of Circulating Monocytes

Liu

Dvornyk

Lü

et al. 2005

Journal of Biological Chemistry

115

128

View full text Add to dashboard Cite

show abstract

“…Osteoblastic cells can secrete MCP-1, MCP-2, and MCP-3 following activation by bone bacterial pathogens in vitro, and these chemokines can in turn recruit and activate monocytes and selectively stimulate subpopulations of lymphocytes and Natural Killer cells (72). Moreover, osteoblastic cells produce other CXC chemokines (GCP-2, IL-8, GRO-␣, GRO-␥, and IP-10) that may play a role in the recruitment and activation of neutrophils (73). Because dlk1 can be produced in the bone marrow by hMSC (15) and CD34ϩ cells (74), it is possible that it can act to amplify these inflammatory responses during infection.…”

Section: Genementioning

confidence: 99%

dlk1/FA1 Regulates the Function of Human Bone Marrow Mesenchymal Stem Cells by Modulating Gene Expression of Pro-inflammatory Cytokines and Immune Response-related Factors

Abdallah

Boissy

Tan

et al. 2007

Journal of Biological Chemistry

View full text Add to dashboard Cite

dlk1/FA1 (delta-like 1/fetal antigen-1) is a member of the epidermal growth factor-like homeotic protein family whose expression is known to modulate the differentiation signals of mesenchymal and hematopoietic stem cells in bone marrow. We have demonstrated previously that Dlk1 can maintain the human bone marrow mesenchymal stem cells (hMSC) in an undifferentiated state. To identify the molecular mechanisms underlying these effects, we compared the basal gene expression pattern in Dlk1-overexpressing hMSC cells (hMSC-dlk1) versus control hMSC (negative for Dlk1 expression) by using Affymetrix HG-U133A microarrays. In response to Dlk1 expression, 128 genes were significantly up-regulated (with >2-fold; p < 0.001), and 24% of these genes were annotated as immune response-related factors, including pro-inflammatory cytokines, in addition to factors involved in the complement system, apoptosis, and cell adhesion. Also, addition of purified FA1 to hMSC up-regulated the same factors in a dose-dependent manner. As biological consequences of up-regulating these immune response-related factors, we showed that the inhibitory effects of dlk1 on osteoblast and adipocyte differentiation of hMSC are associated with Dlk1-induced cytokine expression. Furthermore, Dlk1 promoted B cell proliferation, synergized the immune response effects of the bacterial endotoxin lipopolysaccharide on hMSC, and led to marked transactivation of the NF-B. Our data suggest a new role for Dlk1 in regulating the multiple biological functions of hMSC by influencing the composition of their microenvironment "niche." Our findings also demonstrate a role for Dlk1 in mediating the immune response.

show abstract

“…For example, pre-osteoblasts synthesize the receptor activator of nuclear factor-κb ligand (RANKL) and osteoprotegerin (OPG), which regulate the differentiation and formation of osteoclasts. In return, sphingosine-1-phosphate (S1P), platelet derived growth factor (PDGF) or hepatic growth factor (HGF) secreted by osteoclasts have effects on activation of osteoblasts [24,25,26]; moreover, factors like transforming growth factor beta (TGF-β), bone morphogenetic proteins (BMP), insulin-like growth factor (IGF), collagen, and osteocalcin (OC) secreted and incorporated into the bone matrix by osteoblasts, may get liberated and in some cases even activated by osteoclasts [27]. These examples clearly show that bone remodeling is based on communication and regulated by the balance between osteoclasts and osteoblasts, which also varies at different stages of differentiation [28,29,30].…”

Section: Osteoblast and Osteoclast Interactionmentioning

confidence: 99%

From the Clinical Problem to the Basic Research—Co-Culture Models of Osteoblasts and Osteoclasts

Zhu¹,

Ehnert²,

Rouß³

et al. 2018

IJMS

View full text Add to dashboard Cite

Bone tissue undergoes constant remodeling and healing when fracture happens, in order to ensure its structural integrity. In order to better understand open biological and clinical questions linked to various bone diseases, bone cell co-culture technology is believed to shed some light into the dark. Osteoblasts/osteocytes and osteoclasts dominate the metabolism of bone by a multitude of connections. Therefore, it is widely accepted that a constant improvement of co-culture models with both cell types cultured on a 3D scaffold, is aimed to mimic an in vivo environment as closely as possible. Although in recent years a considerable knowledge of bone co-culture models has been accumulated, there are still many open questions. We here try to summarize the actual knowledge and address open questions.

show abstract

The expression of monocyte chemoattractant protein-1 and other chemokines by osteoblasts

Cited by 54 publications

References 28 publications

A Novel Pathophysiological Mechanism for Osteoporosis Suggested by an in Vivo Gene Expression Study of Circulating Monocytes

A Novel Pathophysiological Mechanism for Osteoporosis Suggested by an in Vivo Gene Expression Study of Circulating Monocytes

dlk1/FA1 Regulates the Function of Human Bone Marrow Mesenchymal Stem Cells by Modulating Gene Expression of Pro-inflammatory Cytokines and Immune Response-related Factors

From the Clinical Problem to the Basic Research—Co-Culture Models of Osteoblasts and Osteoclasts

Contact Info

Product

Resources

About