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 "as col17 defects disrupt keratinocyte-basal lamina adhesion and underlie the disease non-herlitz junctional epidermolysis bullosa" symptom

junctional epidermolysis bullosa

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