Regulation of Embryonic and Postnatal Development by the CSF-1 Receptor

Violeta Chitu, E. R. Stanley

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Macrophages are found in all tissues and regulate tissue morphogenesis during development through trophic and scavenger functions. The colony stimulating factor-1 (CSF-1) receptor (CSF-1R) is the major regulator of tissue macrophage development and maintenance. In combination with receptor activator of nuclear factor κB (RANK), the CSF-1R also regulates the differentiation of the bone-resorbing osteoclast and controls bone remodeling during embryonic and early postnatal development. CSF-1R-regulated macrophages play trophic and remodeling roles in development. Outside the mononuclear phagocytic system, the CSF-1R directly regulates neuronal survival and differentiation, the development of intestinal Paneth cells and of preimplantation embryos, as well as trophoblast innate immune function. Consistent with the pleiotropic roles of the receptor during development, CSF-1R deficiency in most mouse strains causes embryonic or perinatal death and the surviving mice exhibit multiple developmental and functional deficits. The CSF-1R is activated by two dimeric glycoprotein ligands, CSF-1, and interleukin-34 (IL-34). Homozygous . Csf1-null mutations phenocopy most of the deficits of . Csf1r-null mice. In contrast, . Il34-null mice have no gross phenotype, except for decreased numbers of Langerhans cells and microglia, indicating that CSF-1 plays the major developmental role. Homozygous inactivating mutations of the . Csf1r or its ligands have not been reported in man. However, heterozygous inactivating mutations in the . Csf1r lead to a dominantly inherited adult-onset progressive dementia, highlighting the importance of CSF-1R signaling in the brain.

Original languageEnglish (US)
JournalCurrent Topics in Developmental Biology
DOIs
StateAccepted/In press - 2016

Fingerprint

Colony-Stimulating Factor Receptors
Macrophage Colony-Stimulating Factor Receptors
Macrophage Colony-Stimulating Factor
Embryonic Development
Macrophages
Mutation
Paneth Cells
Ligands
Langerhans Cells
Bone Remodeling
Interleukins
Trophoblasts
Microglia
Blastocyst
Osteoclasts
Cytoplasmic and Nuclear Receptors
Morphogenesis
Dementia
Cause of Death
Glycoproteins

Keywords

  • CSF-1
  • CSF-1R
  • IL-34
  • Langerhans cells
  • Macrophages
  • Microglia
  • Neural progenitor cells
  • Osteoclasts
  • Paneth cells
  • Trophoblast cells

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

Cite this

@article{6ddeabed900e48a3a2af8e36757277c2,
title = "Regulation of Embryonic and Postnatal Development by the CSF-1 Receptor",
abstract = "Macrophages are found in all tissues and regulate tissue morphogenesis during development through trophic and scavenger functions. The colony stimulating factor-1 (CSF-1) receptor (CSF-1R) is the major regulator of tissue macrophage development and maintenance. In combination with receptor activator of nuclear factor κB (RANK), the CSF-1R also regulates the differentiation of the bone-resorbing osteoclast and controls bone remodeling during embryonic and early postnatal development. CSF-1R-regulated macrophages play trophic and remodeling roles in development. Outside the mononuclear phagocytic system, the CSF-1R directly regulates neuronal survival and differentiation, the development of intestinal Paneth cells and of preimplantation embryos, as well as trophoblast innate immune function. Consistent with the pleiotropic roles of the receptor during development, CSF-1R deficiency in most mouse strains causes embryonic or perinatal death and the surviving mice exhibit multiple developmental and functional deficits. The CSF-1R is activated by two dimeric glycoprotein ligands, CSF-1, and interleukin-34 (IL-34). Homozygous . Csf1-null mutations phenocopy most of the deficits of . Csf1r-null mice. In contrast, . Il34-null mice have no gross phenotype, except for decreased numbers of Langerhans cells and microglia, indicating that CSF-1 plays the major developmental role. Homozygous inactivating mutations of the . Csf1r or its ligands have not been reported in man. However, heterozygous inactivating mutations in the . Csf1r lead to a dominantly inherited adult-onset progressive dementia, highlighting the importance of CSF-1R signaling in the brain.",
keywords = "CSF-1, CSF-1R, IL-34, Langerhans cells, Macrophages, Microglia, Neural progenitor cells, Osteoclasts, Paneth cells, Trophoblast cells",
author = "Violeta Chitu and Stanley, {E. R.}",
year = "2016",
doi = "10.1016/bs.ctdb.2016.10.004",
language = "English (US)",
journal = "Current Topics in Developmental Biology",
issn = "0070-2153",
publisher = "Academic Press Inc.",

}

TY - JOUR

T1 - Regulation of Embryonic and Postnatal Development by the CSF-1 Receptor

AU - Chitu, Violeta

AU - Stanley, E. R.

PY - 2016

Y1 - 2016

N2 - Macrophages are found in all tissues and regulate tissue morphogenesis during development through trophic and scavenger functions. The colony stimulating factor-1 (CSF-1) receptor (CSF-1R) is the major regulator of tissue macrophage development and maintenance. In combination with receptor activator of nuclear factor κB (RANK), the CSF-1R also regulates the differentiation of the bone-resorbing osteoclast and controls bone remodeling during embryonic and early postnatal development. CSF-1R-regulated macrophages play trophic and remodeling roles in development. Outside the mononuclear phagocytic system, the CSF-1R directly regulates neuronal survival and differentiation, the development of intestinal Paneth cells and of preimplantation embryos, as well as trophoblast innate immune function. Consistent with the pleiotropic roles of the receptor during development, CSF-1R deficiency in most mouse strains causes embryonic or perinatal death and the surviving mice exhibit multiple developmental and functional deficits. The CSF-1R is activated by two dimeric glycoprotein ligands, CSF-1, and interleukin-34 (IL-34). Homozygous . Csf1-null mutations phenocopy most of the deficits of . Csf1r-null mice. In contrast, . Il34-null mice have no gross phenotype, except for decreased numbers of Langerhans cells and microglia, indicating that CSF-1 plays the major developmental role. Homozygous inactivating mutations of the . Csf1r or its ligands have not been reported in man. However, heterozygous inactivating mutations in the . Csf1r lead to a dominantly inherited adult-onset progressive dementia, highlighting the importance of CSF-1R signaling in the brain.

AB - Macrophages are found in all tissues and regulate tissue morphogenesis during development through trophic and scavenger functions. The colony stimulating factor-1 (CSF-1) receptor (CSF-1R) is the major regulator of tissue macrophage development and maintenance. In combination with receptor activator of nuclear factor κB (RANK), the CSF-1R also regulates the differentiation of the bone-resorbing osteoclast and controls bone remodeling during embryonic and early postnatal development. CSF-1R-regulated macrophages play trophic and remodeling roles in development. Outside the mononuclear phagocytic system, the CSF-1R directly regulates neuronal survival and differentiation, the development of intestinal Paneth cells and of preimplantation embryos, as well as trophoblast innate immune function. Consistent with the pleiotropic roles of the receptor during development, CSF-1R deficiency in most mouse strains causes embryonic or perinatal death and the surviving mice exhibit multiple developmental and functional deficits. The CSF-1R is activated by two dimeric glycoprotein ligands, CSF-1, and interleukin-34 (IL-34). Homozygous . Csf1-null mutations phenocopy most of the deficits of . Csf1r-null mice. In contrast, . Il34-null mice have no gross phenotype, except for decreased numbers of Langerhans cells and microglia, indicating that CSF-1 plays the major developmental role. Homozygous inactivating mutations of the . Csf1r or its ligands have not been reported in man. However, heterozygous inactivating mutations in the . Csf1r lead to a dominantly inherited adult-onset progressive dementia, highlighting the importance of CSF-1R signaling in the brain.

KW - CSF-1

KW - CSF-1R

KW - IL-34

KW - Langerhans cells

KW - Macrophages

KW - Microglia

KW - Neural progenitor cells

KW - Osteoclasts

KW - Paneth cells

KW - Trophoblast cells

UR - http://www.scopus.com/inward/record.url?scp=85007472406&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85007472406&partnerID=8YFLogxK

U2 - 10.1016/bs.ctdb.2016.10.004

DO - 10.1016/bs.ctdb.2016.10.004

M3 - Article

C2 - 28236968

AN - SCOPUS:85007472406

JO - Current Topics in Developmental Biology

JF - Current Topics in Developmental Biology

SN - 0070-2153

ER -