Hon Wai Koon

Metalloproteinase-dependent transforming growth factor-alpha release mediates neurotensin-stimulated MAP kinase activation in human colonic epithelial cells.

Metalloproteinases and transforming growth factor-alpha mediate substance P-induced mitogen-activated protein kinase activation and proliferation in human colonocytes.

Neurotensin stimulates interleukin-8 expression through modulation of I kappa B alpha phosphorylation and p65 transcriptional activity: involvement of protein kinase C alpha.

Clostridium difficile toxin B activates the EGF receptor and the ERK/MAP kinase pathway in human colonocytes.

Substance P-stimulated interleukin-8 expression in human colonic epithelial cells involves protein kinase Cdelta activation.

Substance P stimulates cyclooxygenase-2 and prostaglandin E2 expression through JAK-STAT activation in human colonic epithelial cells.

Immunomodulatory properties of substance P: the gastrointestinal system as a model.

Neurotensin stimulates expression of early growth response gene-1 and EGF receptor through MAP kinase activation in human colonic epithelial cells.

Substance P mediates antiapoptotic responses in human colonocytes by Akt activation.

Substance P-mediated expression of the pro-angiogenic factor CCN1 modulates the course of colitis.

Substance P promotes expansion of human mesenteric preadipocytes through proliferative and antiapoptotic pathways.

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis.

Saccharomyces boulardii inhibits EGF receptor signaling and intestinal tumor growth in Apc(min) mice.

Substance P modulates colitis-associated fibrosis.

Insulin-like growth factor-1 receptor transactivation modulates the inflammatory and proliferative responses of neurotensin in human colonic epithelial cells.

Constitutive TL1A (TNFSF15) expression on lymphoid or myeloid cells leads to mild intestinal inflammation and fibrosis.

Cathelicidin signaling via the Toll-like receptor protects against colitis in mice.

Substance P induces CCN1 expression via histone deacetylase activity in human colonic epithelial cells.

Transgenic mice over-expressing ET-1 in the endothelial cells develop systemic hypertension with altered vascular reactivity.

Constitutive TL1A expression under colitogenic conditions modulates the severity and location of gut mucosal inflammation and induces fibrostenosis.

The antimicrobial peptide cathelicidin modulates Clostridium difficile-associated colitis and toxin A-mediated enteritis in mice.

Antimicrobial Peptides and Colitis.