PMID- 9674118
OWN - NLM
STAT- MEDLINE
DCOM- 19980807
LR  - 20151119
IS  - 0301-4681 (Print)
IS  - 0301-4681 (Linking)
VI  - 63
IP  - 2
DP  - 1998 Jun
TI  - Regulation of the level and glycosylation state of plasminogen activator 
      inhibitor type 2 during human keratinocyte differentiation.
PG  - 93-9
AB  - Plasminogen activator inhibitor type 2 (PAI-2) is an unusual member of the serine 
      proteinase inhibitor (serpin) family which has been implicated in the protection 
      of cells from programmed cell death. Human epidermal keratinocytes synthesize 
      large amounts of PAI-2 in two active forms: glycosylated and non-glycosylated. 
      Calcium (Ca2+), a well-known inducer of numerous aspects of keratinocyte terminal 
      differentiation, increases the steady-state levels of PAI-2 mRNA and protein. As 
      the cultures become more differentiated due to longer incubation with Ca2+, the 
      glycosylated form is preferentially elevated. Surprisingly, glycosylated as well 
      as non-glycosylated PAI-2 remains predominantly cell-associated, in a 
      trypsin-inaccessible form and thus most likely inside the cell. Tumor necrosis 
      factor-alpha (TNF-alpha), an inflammatory mediator that induces some markers of 
      keratinocyte differentiation, also increases PAI-2 mRNA and protein levels. 
      Experiments using cultures in which protein kinase C has been downregulated 
      suggest that Ca2+, but not TNF-alpha, acts at least partially through one or more 
      isozymes of this kinase for induction of PAI-2. This is consistent with the 
      finding that the effect of simultaneous addition of Ca2+ plus TNF-alpha is at 
      least additive, compared with addition of either stimulant alone. These data 
      demonstrate that the keratinocyte maintains multiple regulatory pathways for 
      control of PAI-2 expression, at least one of which is related to terminal 
      differentiation.
FAU - Wang, Y
AU  - Wang Y
AD  - Department of Dermatology, University of Pennsylvania, Philadelphia 19106-6142, 
      USA.
FAU - Jensen, P J
AU  - Jensen PJ
LA  - eng
GR  - R01 AR-42998/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Differentiation
JT  - Differentiation; research in biological diversity
JID - 0401650
RN  - 0 (Biomarkers)
RN  - 0 (Plasminogen Activator Inhibitor 2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Biomarkers
MH  - Calcium/*pharmacology
MH  - Cell Differentiation/drug effects
MH  - Cells, Cultured
MH  - Glycosylation
MH  - Humans
MH  - Keratinocytes/cytology/*drug effects
MH  - Plasminogen Activator Inhibitor 2/*metabolism
MH  - Protein Kinase C/*metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1998/07/23 00:00
MHDA- 1998/07/23 00:01
CRDT- 1998/07/23 00:00
PHST- 1998/07/23 00:00 [pubmed]
PHST- 1998/07/23 00:01 [medline]
PHST- 1998/07/23 00:00 [entrez]
AID - S0301-4681(09)60638-1 [pii]
AID - 10.1046/j.1432-0436.1998.6320093.x [doi]
PST - ppublish
SO  - Differentiation. 1998 Jun;63(2):93-9. doi: 10.1046/j.1432-0436.1998.6320093.x.