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EV71 induces VCAM-1 expression via PDGF receptor, PI3-K/Akt, p38 MAPK, JNK and NF-kappaB in vascular smooth muscle cells.
Cell Signal. 2007 Oct; 19(10):2127-37.CS

Abstract

Enterovirus 71 (EV71) is a widespread virus that causes severe and fatal diseases in patients, including circulation failure. The mechanisms underlying EV71-initiated intracellular signaling pathways to influence host cell functions remain unknown. In this study, we identified a requirement for PDGFR, PI3-K/Akt, p38 MAPK, JNK, and NF-kappaB in the regulation of VCAM-1 expression by rat vascular smooth muscle cells (VSMCs) in response to viral infection. EV71 induced VCAM-1 expression in a time- and viral concentration-dependent manner. Infection of VSMCs with EV71 stimulated VCAM-1 expression and phosphorylation of PDGFR, Akt, and p38 MAPK which were attenuated by AG1296, wortmannin, and SB202190, respectively. The phosphorylation of JNK stimulated by EV71 was not detected under present conditions. In contrast, JNK inhibitor SP600125 inhibited EV71-induced VCAM-1 expression. Furthermore, VCAM-1 expression induced by EV71 was significantly attenuated by a selective NF-kappaB inhibitor (helenalin). Consistently, EV71-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha as well as VCAM-1 mRNA expression was blocked by helenalin, AG1296, SB202190, SP600125, wortmannin, and LY294002. Moreover, the involvement of p38 MAPK, PI3-K/Akt, and NF-kappaB in EV71-induced VCAM-1 expression was reveled by that transfection with dominant negative plasmids of p38 MAPK, p85, Akt, NIK, IKK-alpha, and IKK-beta attenuated these responses. These findings suggest that in VSMCs, EV71-induced VCAM-1 expression was mediated through activation of PDGFR, PI3-K/Akt, p38 MAPK, JNK, and NF-kappaB pathways.

Authors+Show Affiliations

Department of Physiology and Pharmacology, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan, Taiwan.No affiliation info availableNo 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

17669626

Citation

Tung, Wei-Hsuan, et al. "EV71 Induces VCAM-1 Expression Via PDGF Receptor, PI3-K/Akt, P38 MAPK, JNK and NF-kappaB in Vascular Smooth Muscle Cells." Cellular Signalling, vol. 19, no. 10, 2007, pp. 2127-37.
Tung WH, Sun CC, Hsieh HL, et al. EV71 induces VCAM-1 expression via PDGF receptor, PI3-K/Akt, p38 MAPK, JNK and NF-kappaB in vascular smooth muscle cells. Cell Signal. 2007;19(10):2127-37.
Tung, W. H., Sun, C. C., Hsieh, H. L., Wang, S. W., Horng, J. T., & Yang, C. M. (2007). EV71 induces VCAM-1 expression via PDGF receptor, PI3-K/Akt, p38 MAPK, JNK and NF-kappaB in vascular smooth muscle cells. Cellular Signalling, 19(10), 2127-37.
Tung WH, et al. EV71 Induces VCAM-1 Expression Via PDGF Receptor, PI3-K/Akt, P38 MAPK, JNK and NF-kappaB in Vascular Smooth Muscle Cells. Cell Signal. 2007;19(10):2127-37. PubMed PMID: 17669626.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - EV71 induces VCAM-1 expression via PDGF receptor, PI3-K/Akt, p38 MAPK, JNK and NF-kappaB in vascular smooth muscle cells. AU - Tung,Wei-Hsuan, AU - Sun,Chi-Chin, AU - Hsieh,Hsi-Lung, AU - Wang,Shyi-Wu, AU - Horng,Jim-Tong, AU - Yang,Chuen-Mao, Y1 - 2007/06/28/ PY - 2007/05/18/received PY - 2007/06/15/accepted PY - 2007/8/3/pubmed PY - 2007/12/7/medline PY - 2007/8/3/entrez SP - 2127 EP - 37 JF - Cellular signalling JO - Cell Signal VL - 19 IS - 10 N2 - Enterovirus 71 (EV71) is a widespread virus that causes severe and fatal diseases in patients, including circulation failure. The mechanisms underlying EV71-initiated intracellular signaling pathways to influence host cell functions remain unknown. In this study, we identified a requirement for PDGFR, PI3-K/Akt, p38 MAPK, JNK, and NF-kappaB in the regulation of VCAM-1 expression by rat vascular smooth muscle cells (VSMCs) in response to viral infection. EV71 induced VCAM-1 expression in a time- and viral concentration-dependent manner. Infection of VSMCs with EV71 stimulated VCAM-1 expression and phosphorylation of PDGFR, Akt, and p38 MAPK which were attenuated by AG1296, wortmannin, and SB202190, respectively. The phosphorylation of JNK stimulated by EV71 was not detected under present conditions. In contrast, JNK inhibitor SP600125 inhibited EV71-induced VCAM-1 expression. Furthermore, VCAM-1 expression induced by EV71 was significantly attenuated by a selective NF-kappaB inhibitor (helenalin). Consistently, EV71-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha as well as VCAM-1 mRNA expression was blocked by helenalin, AG1296, SB202190, SP600125, wortmannin, and LY294002. Moreover, the involvement of p38 MAPK, PI3-K/Akt, and NF-kappaB in EV71-induced VCAM-1 expression was reveled by that transfection with dominant negative plasmids of p38 MAPK, p85, Akt, NIK, IKK-alpha, and IKK-beta attenuated these responses. These findings suggest that in VSMCs, EV71-induced VCAM-1 expression was mediated through activation of PDGFR, PI3-K/Akt, p38 MAPK, JNK, and NF-kappaB pathways. SN - 0898-6568 UR - https://www.unboundmedicine.com/medline/citation/17669626/EV71_induces_VCAM_1_expression_via_PDGF_receptor_PI3_K/Akt_p38_MAPK_JNK_and_NF_kappaB_in_vascular_smooth_muscle_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0898-6568(07)00186-6 DB - PRIME DP - Unbound Medicine ER -