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Involvement of p38 MAPK, JNK, p42/p44 ERK and NF-kappaB in IL-1beta-induced chemokine release in human airway smooth muscle cells.
Respir Med. 2003 Jul; 97(7):811-7.RM

Abstract

Asthma is an inflammatory disease, in which eotaxin, MCP-1 and MCP-3 play a crucial role. These chemokines have been shown to be expressed and produced by IL-1beta-stimulated human airway smooth muscle cells (HASMC) in culture. In the present study we were interested to unravel the IL-1beta-induced signal transduction leading to chemokine production. Using Western blot, we observed an activation of p38 MAPK, JNK kinase and p42/p44 ERK when HASMC were stimulated with IL-1beta. We also observed a significant decrease in the expression and the release of eotaxin, MCP-1 and MCP-3 in the presence of SB203580, an inhibitor of p38 MAPK (71 +/- 6%, P < 0.05, n = 8 and 39 +/- 10% P < 0.01, n = 10 respectively), curcumin, an inhibitor of JNK kinase (83 +/- 4.9% and 88 +/- 3.4% respectively, P < 0.01, n = 4). U0126, an inhibitor of p42/p44 ERK, also produced a significant decrease in chemokine production (46.3 +/- 9%, P < 0.01 n = 10 and 67.8 +/- 12%, P < 0.01, n = 12). Pyrrolydine dithiocarbamate, an inhibitor of NF-kappaB was also able to reduce the eotaxin, MCP-1 and MCP-3 expression and production (50 +/- 13%, P < 0.05, n = 10 and 23 +/- 7%, P < 0.05, n = 12). We conclude that p38 MAPK, JNK kinase, ERK and NF-kappaB are involved in the IL-1beta-induced eotaxin, MCP-1, and MCP-3 expression and release in HASMC.

Authors+Show Affiliations

Lung Transplantation Unit, Department of Respiratory Diseases, University Hospital Gasthuisberg, 49 Herestraat, Leuven B-3000, Belgium.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12854631

Citation

Wuyts, Wim A., et al. "Involvement of P38 MAPK, JNK, P42/p44 ERK and NF-kappaB in IL-1beta-induced Chemokine Release in Human Airway Smooth Muscle Cells." Respiratory Medicine, vol. 97, no. 7, 2003, pp. 811-7.
Wuyts WA, Vanaudenaerde BM, Dupont LJ, et al. Involvement of p38 MAPK, JNK, p42/p44 ERK and NF-kappaB in IL-1beta-induced chemokine release in human airway smooth muscle cells. Respir Med. 2003;97(7):811-7.
Wuyts, W. A., Vanaudenaerde, B. M., Dupont, L. J., Demedts, M. G., & Verleden, G. M. (2003). Involvement of p38 MAPK, JNK, p42/p44 ERK and NF-kappaB in IL-1beta-induced chemokine release in human airway smooth muscle cells. Respiratory Medicine, 97(7), 811-7.
Wuyts WA, et al. Involvement of P38 MAPK, JNK, P42/p44 ERK and NF-kappaB in IL-1beta-induced Chemokine Release in Human Airway Smooth Muscle Cells. Respir Med. 2003;97(7):811-7. PubMed PMID: 12854631.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of p38 MAPK, JNK, p42/p44 ERK and NF-kappaB in IL-1beta-induced chemokine release in human airway smooth muscle cells. AU - Wuyts,Wim A, AU - Vanaudenaerde,Bart M, AU - Dupont,Lieven J, AU - Demedts,Maurits G, AU - Verleden,Geert M, PY - 2003/7/12/pubmed PY - 2003/8/5/medline PY - 2003/7/12/entrez SP - 811 EP - 7 JF - Respiratory medicine JO - Respir Med VL - 97 IS - 7 N2 - Asthma is an inflammatory disease, in which eotaxin, MCP-1 and MCP-3 play a crucial role. These chemokines have been shown to be expressed and produced by IL-1beta-stimulated human airway smooth muscle cells (HASMC) in culture. In the present study we were interested to unravel the IL-1beta-induced signal transduction leading to chemokine production. Using Western blot, we observed an activation of p38 MAPK, JNK kinase and p42/p44 ERK when HASMC were stimulated with IL-1beta. We also observed a significant decrease in the expression and the release of eotaxin, MCP-1 and MCP-3 in the presence of SB203580, an inhibitor of p38 MAPK (71 +/- 6%, P < 0.05, n = 8 and 39 +/- 10% P < 0.01, n = 10 respectively), curcumin, an inhibitor of JNK kinase (83 +/- 4.9% and 88 +/- 3.4% respectively, P < 0.01, n = 4). U0126, an inhibitor of p42/p44 ERK, also produced a significant decrease in chemokine production (46.3 +/- 9%, P < 0.01 n = 10 and 67.8 +/- 12%, P < 0.01, n = 12). Pyrrolydine dithiocarbamate, an inhibitor of NF-kappaB was also able to reduce the eotaxin, MCP-1 and MCP-3 expression and production (50 +/- 13%, P < 0.05, n = 10 and 23 +/- 7%, P < 0.05, n = 12). We conclude that p38 MAPK, JNK kinase, ERK and NF-kappaB are involved in the IL-1beta-induced eotaxin, MCP-1, and MCP-3 expression and release in HASMC. SN - 0954-6111 UR - https://www.unboundmedicine.com/medline/citation/12854631/Involvement_of_p38_MAPK_JNK_p42/p44_ERK_and_NF_kappaB_in_IL_1beta_induced_chemokine_release_in_human_airway_smooth_muscle_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0954-6111(03)00036-2 DB - PRIME DP - Unbound Medicine ER -