Role of the JNK pathway in thrombin-induced ICAM-1 expression in endothelial cells

Miho, Narimasa; Ishida, Takafumi; Kuwaba, Noriko; Ishida, Mari; Shimote-Abe, Keiko; Tabuchi, Kumiko; Oshima, Tetsuya; Yoshizumi, Masao; Chayama, Kazuaki

doi:10.1016/j.cardiores.2005.05.029

Cited by 36 publications

(25 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To evaluate the role of Rho kinase, ECs were pretreated with either vehicle (H 2 O) or 20 M Y27632 for 30 min (19,(22)(23)(24). To evaluate the role of JNK, ECs were pretreated with either vehicle (0.1% DMSO) or 40 M SP600125 for 30 min (25). To evaluate the role of PI3K, ECs were pretreated with either vehicle (0.1% DMSO) or 20 M LY294002 for 30 min (26).…”

Section: Cells Pharmacological Inhibitors and Small-interfering Rnamentioning

confidence: 99%

Activation of Rho Kinase by TNF-α Is Required for JNK Activation in Human Pulmonary Microvascular Endothelial Cells

Mong

Petrulio

Kaufman

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

TNF‐α induces complex signaling events in endothelial cells (ECs), resulting in gene transcription and increased junctional permeability. This study examined the activation of the RhoA/Rho kinase pathway induced by TNF‐α in primary human pulmonary microvascular ECs and its role in EC responses to TNF‐α. Activation of RhoA was induced by TNF‐α within five minutes. This increase in RhoA activity rapidly decreased, and a late activation of RhoA was induced three hours after TNF‐α treatment. This late but not early RhoA activation was associated with its accumulation in focal aggregates near EC edges. TNF‐α also induced Rho kinase activation that was observed within five minutes and lasted for at least three hours. Inhibition of Rho kinase prevented TNF‐α‐induced cytoskeletal changes and permeability increases. TNF‐α also induced activation of JNK that peaked at fifteen minutes and lasted for at least three hours, and inhibition of Rho kinase prevented TNF‐α‐induced early and late JNK activation. Inhibition of JNK activation, however, did not prevent TNF‐α‐induced cytoskeletal changes, suggesting that Rho kinase did not modulate cytoskeletal changes through JNK activation. These data demonstrate that RhoA/Rho kinase pathway is rapidly activated by TNF‐α and regulates several downstream responses that include JNK activation, cytoskeletal changes and increases in permeability. Supported by NIH HL070009.

show abstract

Section: Cells Pharmacological Inhibitors and Small-interfering Rnamentioning

confidence: 99%

Activation of Rho Kinase by TNF-α Is Required for JNK Activation in Human Pulmonary Microvascular Endothelial Cells

Mong

Petrulio

Kaufman

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…RNA isolation and real-time PCR were performed as described previously (16). In brief, cells were lysed in TRIzol (Invitrogen, Carlsbad, USA) and then mixed with chloroform.…”

Section: Rna Isolation and Real-time Pcrmentioning

confidence: 99%

Angiotensin II-Induced Osteopontin Expression in Vascular Smooth Muscle Cells Involves Gq/11, Ras, ERK, Src and Ets-1

et al. 2008

View full text Add to dashboard Cite

“…JNK activation during reperfusion is believed to play a role in hepatocyte apoptosis (Marderstein et al, 2003;Uehara et al, 2004;Uehara et al, 2005). JNK also mediates inflammatory processes by inducing the expression of adhesion molecules (Miho et al, 2005) and inflammatory chemokines/cytokines (Paik et al, 2003;Arndt et al, 2004). Therefore, JNK is thought to play a key role in hepatic I/R injury.…”

Section: Introductionmentioning

confidence: 99%

SP600125, a selective JNK inhibitor, aggravates hepatic ischemia-reperfusion injury

Lee

Kim²,

Lee³

2006

Exp Mol Med

View full text Add to dashboard Cite

Abstractc-Jun N-terminal kinase (JNK) is activated during hepatic reperfusion, and JNK inhibitors are known to protect other major organs from ischemia-reperfusion (I/R) injury. We attempted to determine the effect of SP600125, a JNK inhibitor, on hepatic I/R injury using a partial ischemia model in mice. Compared to a vehicle-treated group, the SP600125-treated group showed a greater increase in serum ALT levels 24 h after reperfusion with more severe parenchymal destruction and leukocyte infiltration. Similarly, tissue myeloperoxidase and malondialdehyde levels were higher in the SP600125-treated group, and chemokine expression was also higher in the SP600125-treated group. These data, which are contradictory to previous results, indicate that JNK inhibition by SP600125 may be harmful in hepatic I/R injury. Therefore, care must be taken when investigating the therapeutic use of JNK inhibitors in hepatic I/R injury, especially in the context of the effects of JNK inhibition on inflammatory infiltration.

show abstract

Role of the JNK pathway in thrombin-induced ICAM-1 expression in endothelial cells

Abstract: These data suggest that, in concert with NF-kappaB, JNK regulates thrombin-induced ICAM-1 expression by a mechanism that is dependent on Galpha(q), Gbetagamma, Ras, Rac1 and the Src kinase family.

Cited by 36 publications

References 40 publications

Activation of Rho Kinase by TNF-α Is Required for JNK Activation in Human Pulmonary Microvascular Endothelial Cells

Activation of Rho Kinase by TNF-α Is Required for JNK Activation in Human Pulmonary Microvascular Endothelial Cells

Angiotensin II-Induced Osteopontin Expression in Vascular Smooth Muscle Cells Involves Gq/11, Ras, ERK, Src and Ets-1

SP600125, a selective JNK inhibitor, aggravates hepatic ischemia-reperfusion injury

Contact Info

Product

Resources

About