Collagen XVII participates in keratinocyte adhesion to collagen IV, and in p38MAPK-dependent migration and cell signaling.

[junctional epidermolysis bullosa]

Collagen XVII (COL 17 ) participates in keratinocyte adhesion and possibly migration , as COL 17 defects disrupt keratinocyte-basal lamina adhesion and underlie the disease non-Herlitz junctional epidermolysis bullosa . Using small interference RNA (siRNA ) to knock down COL 17 expression in HaCaT cells , we assessed cell characteristics , including adhesion , migration , and signaling . Control and siRNA-transfected keratinocytes showed no difference in adhesion on plastic dishes after incubation for 8 hours in serum-free keratinocyte-growth medium ; however , when grown on collagen IV alone or BD matrigel (containing collagen IV and laminin isoforms ), COL 17 -deficient cells showed significantly reduced adhesion compared with controls (P <0 .01 ), and mitogen-activated protein kinase (MAPK )/ERK kinase (MEK )1 /2 and MAPK showed reduced phosphorylation . Furthermore , COL 17 -deficient HaCaT cells plated on plastic exhibited reduced motility that was p 38 MAPK -dependent (after addition of the p 38 MAPK inhibitor SB 203580 ). Together , these results suggest that COL 17 has significantly wider signaling roles than were previously thought , including the involvement of COL 17 in keratinocyte adhesion to collagen IV , in p 38 MAPK -dependent cell migration , and multiple cell signaling events pertaining to MEK 1 /2 phosphorylation .

Diseases
Validation

Diseases presenting "deficient cells" symptom

child syndrome

esophageal adenocarcinoma

gm1 gangliosidosis

junctional epidermolysis bullosa

kindler syndrome

lymphangioleiomyomatosis

neonatal adrenoleukodystrophy

werner syndrome

You can validate or delete this automatically detected symptom