PMID- 10095777
OWN - NLM
STAT- MEDLINE
DCOM- 19990426
LR  - 20190620
IS  - 0014-2956 (Print)
IS  - 0014-2956 (Linking)
VI  - 260
IP  - 2
DP  - 1999 Mar
TI  - Isolation of the CXC chemokines ENA-78, GRO alpha and GRO gamma from tumor cells 
      and leukocytes reveals NH2-terminal heterogeneity. Functional comparison of
      different natural isoforms.
PG  - 421-9
AB  - Chemokines are a family of chemotactic peptides affecting leukocyte migration
      during the inflammatory response. Post-translational modification of chemokines
      has been shown to affect their biological potency. Here, the isolation and
      identification of natural isoforms of the neutrophil chemoattractants GRO alpha
      and GRO gamma and the epithelial-cell-derived neutrophil attractant-78 (ENA-78), 
      is reported. Cultured tumor cells produced predominantly intact chemokine forms, 
      whereas peripheral blood monocytes secreted mainly NH2-terminally truncated
      forms. The order of neutrophil chemotactic potency of these CXC chemokines was
      GRO alpha > GRO gamma > ENA-78 both for intact and truncated forms. However,
      truncated GRO alpha (4,5,6-73), GRO gamma (5-73) and ENA-78(8,9-78) were 30-fold,
      fivefold and threefold more active than the corresponding intact chemokine. As a 
      consequence, truncated GRO alpha (4,5,6-73) was 300-fold more potent than intact 
      ENA-78 indicating that both the type of chemokine and its mode of processing
      determine the chemotactic potency. Similar observations were made when intact and
      truncated GRO alpha, GRO gamma and ENA-78 were compared for their capacity to
      induce an increase in the intracellular calcium concentration in neutrophilic
      granulocytes, and to desensitize the calcium response towards the CXC chemokine
      granulocyte chemotactic protein-2 (GCP-2). It must be concluded that
      physiological proteolytic cleavage of CXC chemokines in general enhances the
      inflammatory response, whereas for CC chemokines NH2-terminal processing mostly
      results in reduced chemotactic potency.
FAU - Wuyts, A
AU  - Wuyts A
AD  - Rega Institute for Medical Research, Laboratory of Molecular Immunology,
      University of Leuven, Belgium.
FAU - Govaerts, C
AU  - Govaerts C
FAU - Struyf, S
AU  - Struyf S
FAU - Lenaerts, J P
AU  - Lenaerts JP
FAU - Put, W
AU  - Put W
FAU - Conings, R
AU  - Conings R
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  - England
TA  - Eur J Biochem
JT  - European journal of biochemistry
JID - 0107600
RN  - 0 (CXCL1 protein, human)
RN  - 0 (CXCL5 protein, human)
RN  - 0 (CXCL6 protein, human)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Chemokine CXCL5)
RN  - 0 (Chemokine CXCL6)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Growth Inhibitors)
RN  - 0 (Growth Substances)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-8)
RN  - 0 (Neoplasm Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Chemokine CXCL1
MH  - Chemokine CXCL5
MH  - Chemokine CXCL6
MH  - Chemokines, CXC/*isolation & purification/metabolism
MH  - Chemotactic Factors/*isolation & purification/metabolism
MH  - *Chemotaxis, Leukocyte
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Growth Inhibitors/*isolation & purification/metabolism
MH  - Growth Substances/*isolation & purification/metabolism
MH  - Humans
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Interleukin-8/*analogs & derivatives/isolation & purification/metabolism
MH  - Molecular Sequence Data
MH  - Neoplasm Proteins/*isolation & purification/metabolism
MH  - *Neutrophil Activation
MH  - Signal Transduction
MH  - Tumor Cells, Cultured
EDAT- 1999/03/30 00:00
MHDA- 1999/03/30 00:01
CRDT- 1999/03/30 00:00
PHST- 1999/03/30 00:00 [pubmed]
PHST- 1999/03/30 00:01 [medline]
PHST- 1999/03/30 00:00 [entrez]
AID - 10.1046/j.1432-1327.1999.00166.x [doi]
PST - ppublish
SO  - Eur J Biochem. 1999 Mar;260(2):421-9. doi: 10.1046/j.1432-1327.1999.00166.x.