Cytokines/ Chemical
Compounds |
Possible mechanism |
Reference |
Norepinephrine |
Wnt signaling pathway: Protein kinase C (PKC)
activated, stimulates a G reduce the transient outward K+ current |
[3] |
FGFs, BMP |
Wnt extra cellular factors: heparan sulfate proteoglycans. The polysaccharide chains of heparan sulfate bind to FGFs, Wnts and BMPs |
[3] |
Hepatocyte growth factor(HGF) |
1. Ras-ERK1/2 MAPK: mitogenic and morphogenic
2. PI3K/Akt: mitogenic and antiapoptotic
3. p38 MAPK: blocking cells in theG0-G1 phase |
[8] |
Transforming growth factor-β |
Gadd45b promote activated by TGF-β
through the action of Smad2, Smad3, and Smad4 |
[9] |
OSM |
gp130 induces gene-expression, followed byparacrine secretion |
[7] |
Epidermal growth factor(EGF)
Dexamethasone |
Lead to ERK1/2 phosphorylation |
[10] |
Granulocyte macrophage colony stimulating factor
(GM-CSF) |
Induction of suppressor leukocytes: iNOS,Tcell CD3-δ |
[11] |
Stromal
derived |
Ligand forthe chemokine receptor CXCR4.
CXCR4-mediated signaling regulates cell |
[12] |
factor-1a
(SDF-1a) |
migration and apoptosis |
|
Retinoic acid |
Acting through RARγ up-regulation of hepaticCB1R mediates the auto induction of CB1R expression by endo cannabinoids |
[13] |
Sodium butyrate |
1. Promotes protein acetylation at targets : H3K9
2. Accelerates promoter DNA demethylation, expression of pluripotency-associatedgenes POU5F1/OCT4 and DPPA2 |
[14] |
Dimethyl sulfoxide |
Decreases membrane thickening, inducing apoptosis and differentiation |
[15] |