PAR1
|
Enterocytes |
Increase permeability, apoptosis, chloride secretion, prostaglandin release |
|
Human colon cancer epithelium |
Proliferation and motility |
|
Myenteric neurons |
Suppression of fast excitatory postsynaptic potential |
|
Submucosal neurons |
Inhibition of chloride secretion, |
|
Fibroblasts |
Prostaglandin release |
|
Mast cells |
|
|
Smooth muscle |
Relaxation/contraction |
|
Endothelium |
Gap formation |
PAR2
|
Enterocytes |
Chloride secretion, prostaglandin production, eicosanoid production |
|
Human colon cancer epithelium |
Proliferation |
|
Myenteric neurons |
Neuropeptide release, increased excitability, suppression of fast excitatory postsynaptic potential |
|
Submucosal neurons |
Neuropeptide release, stimulate epithelial ion secretion, hyperexcitability |
|
Fibroblasts |
Prostaglandin release, proliferation |
|
Mast cells |
|
|
Smooth muscle |
Relaxation/contraction |
|
Pancreatic duct epithelium |
Ion channel activation |
|
Pancreatic acinar cells |
Amylase secretion |
|
Endothelium/leukocyte interface |
Rolling, adhesion, transmigration, gap formation |
PAR3
|
Detected by RT–PCR in whole GI tissues (stomach and small intestine), but unidentified cell type |
|
PAR4
|
Enterocytes |
|
|
Submucosa |
Contraction of longitudinal muscle |
|
Enteric neurons |
Depolarization |
|
Endothelium/leukocyte interface |
Rolling, adhesion, transmigration |