PMID- 8717151
OWN - NLM
STAT- MEDLINE
DCOM- 19961022
LR  - 20190726
IS  - 0028-1298 (Print)
IS  - 0028-1298 (Linking)
VI  - 353
IP  - 2
DP  - 1996 Jan
TI  - Stimulation of histamine H2- (and H1)-receptors activates Ca2+ influx in 
      all-trans-retinoic acid-differentiated HL-60 cells independently of phospholipase 
      C or adenylyl cyclase.
PG  - 123-9
AB  - In human neutrophils, histamine H2-receptors mediate activation of adenylyl 
      cyclase (AC) and inhibition of N-formyl-L-methionyl-L-leucyl-L-phenylalanine 
      (FMLP)-induced superoxide anion (O2-) formation, and in HL-60 promyelocytes, 
      H2-receptors mediate parallel activation of AC, phospholipase C (PLC) and 
      non-selective cation (NSC) channels. As all-trans-retinoic acid (RA) is 
      successfully used in the differentiation therapy of acute promyelocytic 
      leukaemia, we studied signal transduction in RA-differentiated HL-60 cells. 
      Histamine and the H2-receptor agonist, impromidine, induced both rises in cAMP 
      levels and cytosolic Ca2+ ([Ca2+]i). Substances acting at post-receptor sites to 
      increase cAMP did not increase [Ca2+]i. H2- but not H1-receptor antagonists 
      inhibited histamine-induced cAMP accumulation and rises in [Ca2+]i were more 
      effectively inhibited by H2- than by H1-receptor antagonists. Histamine-induced 
      rises in [Ca2+]i were completely dependent on the presence of extracellular Ca2+ 
      and were abolished by the blocker of NSC channels, Gd3+, but were resistant to 
      inhibition by pertussis toxin. Unlike FMLP, histamine did not activate PLC. The 
      effects of FMLP on [Ca2+]i were less sensitive to blockade by Gd3+ than those of 
      histamine, and there was no cross-desensitization between the two stimuli. FMLP, 
      but not histamine, inhibited transiently thapsigargin-induced rises in [Ca2+]. 
      Taken together, our results show that histamine activates AC-mediated cAMP 
      accumulation in RA-differentiated HL-60 cells via H2-receptors and NSC 
      channel-mediated Ca2+ influx via H2- (and H1)-receptors. Histamine-induced NSC 
      channel activation is not the consequence of AC- or PLC stimulation and occurs, 
      directly or indirectly, via pertussis toxin-insensitive guanine 
      nucleotide-binding proteins. FMLP and histamine activate Ca2+ influx by different 
      mechanisms. There are similarities in H2-receptor-mediated signal transduction 
      between RA-differentiated HL-60 cells and HL-60 promyelocytes and differences 
      between the former cells and neutrophils, indicating that RA-differentiated HL-60 
      cells must be considered as partially immature.
FAU - Burde, R
AU  - Burde R
AD  - Institut fur Pharmakologie, Universitatsklinikum Benjamin Franklin, Berlin, 
      Germany.
FAU - Seifert, R
AU  - Seifert R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Naunyn Schmiedebergs Arch Pharmacol
JT  - Naunyn-Schmiedeberg's archives of pharmacology
JID - 0326264
RN  - 0 (Receptors, Histamine)
RN  - 5688UTC01R (Tretinoin)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 4.6.1.1 (Adenylyl Cyclases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenylyl Cyclases/metabolism
MH  - Calcium/*metabolism
MH  - Cyclic AMP/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - HL-60 Cells/*metabolism
MH  - Humans
MH  - Receptors, Histamine/*metabolism
MH  - Tretinoin/*metabolism
MH  - Type C Phospholipases/*metabolism
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.1007/BF00168748 [doi]
PST - ppublish
SO  - Naunyn Schmiedebergs Arch Pharmacol. 1996 Jan;353(2):123-9. doi: 
      10.1007/BF00168748.