PMID- 11789669
OWN - NLM
STAT- MEDLINE
DCOM- 20020716
LR  - 20191105
IS  - 1567-5769 (Print)
IS  - 1567-5769 (Linking)
VI  - 2
IP  - 1
DP  - 2002 Jan
TI  - Involvement of mitogen-activated protein kinases in the signal transduction 
      pathway of bone marrow-derived macrophage activation in response to in vitro 
      treatment with thymosin alpha 1.
PG  - 47-58
AB  - Thymosin alpha 1 (Talpha1), a 28-amino acid, acidic thymic peptide, is a 
      promising natural biological response modifier (BRM), which augments and 
      regulates the immune network and is thought to be immunostimulatory also. 
      Recently, we have reported the ability of Talpha1 to activate macrophages to 
      tumoricidal state. In the present investigation, the activation of the p42/44 MAP 
      kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro 
      treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been 
      demonstrated. The activation and expression of phospho-p42/44 MAPK was dose as 
      well as time dependent with maximum expression occurring at 5-15 min following 
      stimulation with 100 ng/ml of Talpha1. The expression of phospho-p42/44 MAPK was 
      inhibited by the MAPK inhibitor, PD98059, pertussis toxin (PTX), tyrosine kinase 
      inhibitor-genistein and P13K inhibitor-wortmannin. Talpha1-induced BMDM 
      tumoricidal functions like the production of NO and TNF-alpha, the key mediator 
      molecules of macrophage cytotoxicity, were also inhibited by the MAPK inhibitor, 
      PD98059, in a dose-dependent manner. These observations suggest that p42/44 MAPK 
      activation is one of the essential signaling events triggered by Talpha1 and may 
      be responsible for the in vitro activation of BMDMs.
FAU - Sodhi, Ajit
AU  - Sodhi A
AD  - School of Biotechnology, Banaras Hindu University, Varanasi, India. 
      ajit.sodhi@lycos.com
FAU - Paul, Saki
AU  - Paul S
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indicators and Reagents)
RN  - 0 (Nitrates)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 61512-21-8 (Thymosin)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - W0B22ISQ1C (Thymalfasin)
SB  - IM
MH  - Adjuvants, Immunologic/*pharmacology
MH  - Animals
MH  - Bone Marrow Cells/drug effects/*immunology/metabolism
MH  - Cell Differentiation/drug effects
MH  - Cell Separation
MH  - Cells, Cultured
MH  - Culture Media, Conditioned
MH  - Enzyme Inhibitors/pharmacology
MH  - GTP-Binding Proteins/metabolism
MH  - Indicators and Reagents
MH  - Macrophages/drug effects/*immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Nitrates/metabolism
MH  - Phosphorylation
MH  - Protein-Tyrosine Kinases/antagonists & inhibitors
MH  - RNA, Messenger/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/*drug effects
MH  - Thymalfasin
MH  - Thymosin/*analogs & derivatives/*pharmacology
MH  - Tumor Necrosis Factor-alpha/biosynthesis
EDAT- 2002/01/16 10:00
MHDA- 2002/07/18 10:01
CRDT- 2002/01/16 10:00
PHST- 2002/01/16 10:00 [pubmed]
PHST- 2002/07/18 10:01 [medline]
PHST- 2002/01/16 10:00 [entrez]
AID - S1567-5769(01)00139-4 [pii]
AID - 10.1016/s1567-5769(01)00139-4 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2002 Jan;2(1):47-58. doi: 10.1016/s1567-5769(01)00139-4.