Premium
C‐terminal fragment of parathyroid hormone‐related protein, PTHrP‐(107–111), stimulates membrane‐associated protein kinase C activity and modulates the proliferation of human and murine skin keratinocytes
Author(s) -
Whitfield James F.,
Isaacs Richard J.,
Jouishomme Hervé,
MacLean Susanne,
Chakravarthy Balu R.,
Morley Paul,
Barisoni Dino,
Regalia Elisabetta,
Armato Ubaldo
Publication year - 1996
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199601)166:1<1::aid-jcp1>3.0.co;2-t
Subject(s) - parathyroid hormone related protein , keratinocyte , protein kinase c , parathyroid hormone , adenylyl cyclase , microbiology and biotechnology , dna synthesis , protein kinase a , cell growth , chemistry , signal transduction , kinase , endocrinology , medicine , biology , calcium , dna , in vitro , biochemistry
Low concentrations of the C‐terminal parathyroid hormone‐related protein (PTHrP) fragments, PTHrP‐(107–111) and PTHrP‐(107–139), stimulated membrane‐associated protein kinase Cs (PKCs), but not adenylyl cyclase or an internal Ca 2+ surge, in early passage human skin keratinocytes and BALB/MK‐2 murine skin keratinocytes. The fragment maximally stimulated membrane‐associated PKCs in BALB/MK‐2 cells at 5 × 10 −9 to 10 −8 M. The maximally PKC‐stimulating concentrations of PTHrP‐(107–111) also stopped or stimulated BALB/MK‐2 keratinocyte proliferation depending on whether the cells were, respectively, cycling or quiescent at the time of exposure. Thus, just one brief (30‐minute) pulse of 10 −8 M PTHrP‐(107–111) stopped the proliferation of BALB/MK‐2 keratinocytes for at least 5 days. On the other hand, daily 30‐minute pulses of 10 −8 M PTHrP‐(107–111) started and then maintained the proliferation of initially quiescent BALB/MK‐2 cells. Similarly PTHrP‐(107–111) inhibited DNA synthesis by cycling primary adult human keratinocytes, but it stimulated DNA synthesis by quiescent human keratinocytes. © 1996, Government of Canada. Exclusive worldwide publication rights in the article have been transferred to Wiley‐Liss, Inc., in perpetuity.