Editing Granulocyte colony-stimulating factor (section)

== Biological function ==
G-CSF is produced by [[endothelium]], [[macrophage]]s, and a number of other [[immune system|immune]] cells. The natural human glycoprotein exists in two forms, a 174- and 177-[[amino acid|amino-acid]]-long [[protein]] of molecular weight 19,600&nbsp;grams per [[Mole (unit)|mole]]. The more-abundant and more-active 174-amino acid form has been used in the development of pharmaceutical products by [[recombinant DNA]] (rDNA) technology.<ref name=":0">{{cite journal | vauthors = Bendall LJ, Bradstock KF | title = G-CSF: From granulopoietic stimulant to bone marrow stem cell mobilizing agent | journal = Cytokine & Growth Factor Reviews | volume = 25 | issue = 4 | pages = 355–367 | date = August 2014 | pmid = 25131807 | doi = 10.1016/j.cytogfr.2014.07.011 | doi-access = free }}</ref>

;White blood cells: The [[Granulocyte colony-stimulating factor receptor|G-CSF-receptor]] is present on precursor cells in the [[bone marrow]], and, in response to stimulation by G-CSF, initiates proliferation and [[Cellular differentiation|differentiation]] into mature [[granulocyte]]s. G-CSF stimulates the survival, proliferation, differentiation, and function of [[neutrophil precursor]]s and mature [[neutrophil]]s. G-CSF regulates them using [[JAK-STAT signaling pathway|Janus kinase (JAK)/signal transducer and activator of transcription (STAT)]] and Ras/[[mitogen-activated protein kinase]] (MAPK) and [[phosphatidylinositol 3-kinase]] (PI3K)/[[protein kinase B]] (Akt) signal transduction pathway.{{citation needed|date=February 2024}}

;Hematopoietic System: G-CSF is also a potent inducer of [[hematopoietic stem cell]] (HSC) mobilization from the bone marrow into the bloodstream, although it has been shown that it does not directly affect the hematopoietic progenitors that are mobilized.<ref name="pmid11953662">{{cite journal | vauthors = Thomas J, Liu F, Link DC | title = Mechanisms of mobilization of hematopoietic progenitors with granulocyte colony-stimulating factor | journal = Current Opinion in Hematology | volume = 9 | issue = 3 | pages = 183–189 | date = May 2002 | pmid = 11953662 | doi = 10.1097/00062752-200205000-00002 | s2cid = 5774130 }}</ref>

;Neurons: G-CSF can also act on neuronal cells as a neurotrophic factor. Indeed, its receptor is expressed by neurons in the brain and spinal cord. The action of G-CSF in the central nervous system is to induce [[neurogenesis]], to increase the [[neuroplasticity]] and to counteract [[apoptosis]].<ref name="pmid16007267">{{cite journal | vauthors = Schneider A, Krüger C, Steigleder T, Weber D, Pitzer C, Laage R, Aronowski J, Maurer MH, Gassler N, Mier W, Hasselblatt M, Kollmar R, Schwab S, Sommer C, Bach A, Kuhn HG, Schäbitz WR | title = The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis | journal = The Journal of Clinical Investigation | volume = 115 | issue = 8 | pages = 2083–2098 | date = August 2005 | pmid = 16007267 | pmc = 1172228 | doi = 10.1172/JCI23559 }}</ref><ref name="pmid18835867">{{cite journal | vauthors = Pitzer C, Krüger C, Plaas C, Kirsch F, Dittgen T, Müller R, Laage R, Kastner S, Suess S, Spoelgen R, Henriques A, Ehrenreich H, Schäbitz WR, Bach A, Schneider A | title = Granulocyte-colony stimulating factor improves outcome in a mouse model of amyotrophic lateral sclerosis | journal = Brain | volume = 131 | issue = Pt 12 | pages = 3335–3347 | date = December 2008 | pmid = 18835867 | pmc = 2639207 | doi = 10.1093/brain/awn243 }}</ref> These properties are currently under investigations for the development of treatments of neurological diseases such as [[cerebral ischemia]].<ref>{{cite journal | vauthors = England TJ, Sprigg N, Alasheev AM, Belkin AA, Kumar A, Prasad K, Bath PM | title = Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis | journal = Scientific Reports | volume = 6 | issue = 1 | pages = 36567 | date = November 2016 | pmid = 27845349 | pmc = 5109224 | doi = 10.1038/srep36567 | bibcode = 2016NatSR...636567E }}</ref>