PMID- 10570306
OWN - NLM
STAT- MEDLINE
DCOM- 19991220
LR  - 20220311
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 163
IP  - 11
DP  - 1999 Dec 1
TI  - NH2- and COOH-terminal truncations of murine granulocyte chemotactic protein-2
      augment the in vitro and in vivo neutrophil chemotactic potency.
PG  - 6155-63
AB  - Chemokines are important mediators of leukocyte migration during the inflammatory
      response. Post-translational modifications affect the biological potency of
      chemokines. In addition to previously identified NH2-terminally truncated forms, 
      COOH-terminally truncated forms of the CXC chemokine murine granulocyte
      chemotactic protein-2 (GCP-2) were purified from conditioned medium of stimulated
      fibroblasts. The truncations generated 28 natural murine GCP-2 isoforms
      containing 69-92 residues, including most intermediate forms. Both NH2- and
      COOH-terminal truncations of GCP-2 resulted in enhanced chemotactic potency for
      human and murine neutrophils in vitro. The truncated isoform GCP-2(9-78) was
      30-fold more potent than intact GCP-2(1-92)/LPS-induced CXC chemokine (LIX) at
      inducing an intracellular calcium increase in human neutrophils. After
      intradermal injection in mice, GCP-2(9-78) was also more effective than
      GCP-2(1-92)/LIX at inducing neutrophil infiltration. Similar to human IL-8 and
      GCP-2, murine GCP-2(9-78) and macrophage inflammatory protein-2 (MIP-2) induced
      calcium increases in both CXCR1 and CXCR2 transfectants. Murine GCP-2(9-78) could
      desensitize the calcium response induced by MIP-2 in human neutrophils and vice
      versa. Furthermore, MIP-2 and truncated GCP-2(9-78), but not intact
      GCP-2(1-92)/LIX, partially desensitized the calcium response to human IL-8 in
      human neutrophils. Taken together, these findings point to an important role of
      post-translationally modified GCP-2 to replace IL-8 in the mouse.
FAU - Wuyts, A
AU  - Wuyts A
AD  - Laboratories ofMolecular Immunology and Immunobiology, Rega Institute for Medical
      Research, and Laboratory for Developmental Physiology and Molecular Biology,
      Zoological Institute, University of Leuven, Leuven, Belgium.
      anja.wuyts@rega.kuleuven.ac.be
FAU - D'Haese, A
AU  - D'Haese A
FAU - Cremers, V
AU  - Cremers V
FAU - Menten, P
AU  - Menten P
FAU - Lenaerts, J P
AU  - Lenaerts JP
FAU - De Loof, A
AU  - De Loof A
FAU - Heremans, H
AU  - Heremans H
FAU - Proost, P
AU  - Proost P
FAU - Van Damme, J
AU  - Van Damme J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antigens, CD)
RN  - 0 (CXCL6 protein, human)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemokine CXCL6)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Monokines)
RN  - 0 (Peptide Fragments)
RN  - 0 (Protein Isoforms)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (Receptors, Interleukin-8A)
RN  - 0 (Receptors, Interleukin-8B)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Antigens, CD/genetics
MH  - Calcium Signaling
MH  - Chemokine CXCL2
MH  - Chemokine CXCL6
MH  - Chemokines, CXC/isolation & purification/*pharmacology
MH  - *Chemotaxis, Leukocyte
MH  - Humans
MH  - Mice
MH  - Molecular Sequence Data
MH  - Monokines/pharmacology
MH  - Neutrophil Infiltration
MH  - Neutrophils/*drug effects
MH  - Peptide Fragments
MH  - Protein Isoforms/isolation & purification/pharmacology
MH  - Receptors, Chemokine/genetics
MH  - Receptors, Interleukin/genetics
MH  - Receptors, Interleukin-8A
MH  - Receptors, Interleukin-8B
MH  - Sequence Alignment
MH  - Sequence Deletion
MH  - Species Specificity
EDAT- 1999/11/26 00:00
MHDA- 1999/11/26 00:01
CRDT- 1999/11/26 00:00
PHST- 1999/11/26 00:00 [pubmed]
PHST- 1999/11/26 00:01 [medline]
PHST- 1999/11/26 00:00 [entrez]
AID - ji_v163n11p6155 [pii]
PST - ppublish
SO  - J Immunol. 1999 Dec 1;163(11):6155-63.