Fluid shear stress inhibits TNF-α activation of JNK but not ERK1/2 or p38 in human umbilical vein endothelial cells: Inhibitory crosstalk among MAPK family members

Surapisitchat, James; Hoefen, Ryan; Pi, Xinchun; Yoshizumi, Masanori; Yan, Chen; Berk, Bradford C.

doi:10.1073/pnas.101134098

Cited by 209 publications

(159 citation statements)

References 39 publications

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“…Suppressed PKB/Akt activation enhanced TNF-induced JNK activation, but JNK activity was not required for HUVEC death. Our results suggest that the observed suppression of TNF-induced JNK activation in endothelial cells induced by shear stress (Surapisitchat et al, 2001) may be due to integrin engagement, because shear stress is detected by integrins at the luminal surface (Shyy and Chien, 2002).…”

Section: Discussionmentioning

confidence: 69%

Distinctive role of integrin-mediated adhesion in TNF-induced PKB/Akt and NF-κB activation and endothelial cell survival

Bieler¹,

Hasmim²,

Monnier³

et al. 2007

Oncogene

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Section: Discussionmentioning

confidence: 69%

Distinctive role of integrin-mediated adhesion in TNF-induced PKB/Akt and NF-κB activation and endothelial cell survival

Bieler¹,

Hasmim²,

Monnier³

et al. 2007

Oncogene

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“…Shear flow-induced STAT3 inactivation may attenuate the IL-6-triggered responses. Presheared ECs have been shown to inhibit subsequent tumor necrosis factorinduced responses (10,11). Our findings may provide new perspectives on the mechanisms of how shear flow protects ECs from cytokine-induced responses.…”

Section: Discussionmentioning

confidence: 99%

Shear Flow Attenuates Serum-induced STAT3 Activation in Endothelial Cells

Hsieh

Chao

Wang

2003

Journal of Biological Chemistry

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ERK1/2 is involved in shear stress-and cyclic strain-induced early growth response-1 expression (5, 6). We have shown that genes such as monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule (ICAM-1), and c-fos can be induced by hemodynamic forces (7-9). The induction of these genes appears to be a redox-sensitive mechanism because an increased reactive oxygen species is required for this gene induction (7-9). Recent studies indicate that ECs under conditions of shear flow inhibit tumor necrosis factor-and H 2 O 2 -induced responses (10 -12). A recent study (13) has nicely demonstrated an induction of antioxidant response element-mediated genes in ECs exposed to laminar flow. Furthermore, shear flow has been shown to inhibit endothelial proliferation via the induction of growth arrest proteins GADD45 and p21, as well as a decrease in phosphorylation of Rb protein (14). Thus, laminar shear flow appears to play an essential role by protecting ECs from inflammatory responses and endothelial proliferation. However, the detailed mechanisms involved in this shear flowinduced protection remain unclear.Signal transducers and activators of transcriptions (STAT) are a family of functionally related proteins that play key roles in a variety of biological activities. Among these STATs, STAT3 is preferentially activated by interleukin-6 (IL-6) or other related cytokines and is required for gp130-mediated cell-survival signals (15,16). STAT3 has been intensively studied for its role in cell growth, differentiation, apoptosis, transformation, inflammation, and immune response. STAT3 is activated by tyrosine phosphorylation at a single site (Tyr-705) and by serine phosphorylation at 727 (Ser-727). Tyrosine phosphorylation of STAT3 in response to cytokine stimulation is mediated by a Janus kinase, and Src family members have been widely studied (17)(18)(19). Tyrosine phosphorylation is required for STAT3 dimerization, nuclear translocation, and DNA binding. For phosphorylation at Ser-727, there is still controversy in identifying the serine kinases. Activation of kinases, including ERK, JNK, and P38, leading to serine phosphorylation in STAT3 has been documented (16). Ser-727 phosphorylation is involved in STAT3 transcriptional activation. However, there is evidence for a negative role for serine phosphorylation. It has been shown that Ser-727 phosphorylation negatively modulates tyrosine phosphorylation (16,20,21). In addition to this cytokine-induced STAT activation, the receptor protein-tyrosine kinase-mediated activation of STAT remains elusive. Recent studies suggest that STAT3 in ECs can be activated by growth factors such as vascular endothelial growth factor (22), basic fibroblast growth factor (23), granulocyte-macrophase

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“…Western Blots and MAPK Antibody Array Analysis-Western blots were performed using standard protocols and were analyzed using the National Institutes of Health Scion software (27) Electrophoretic Mobility Shift Assay-The electrophoretic mobility shift assay protocol has been described previously (28). We used the consensus binding sequence (underlined) for NF-B (5Ј-AGTTGAGGGGACTTTCCCAGG C-3Ј prelabeled with an infrared fluorophore (Licor, Lincoln, NE).…”

Section: Methodsmentioning

confidence: 99%

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

Shaik

Soltau

Chaturvedi

et al. 2009

Journal of Biological Chemistry

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CXC chemokines with a glutamate-leucine-arginine (ELR) tripeptide motif (ELR؉ CXC chemokines) play an important role in leukocyte trafficking into the tissues. For reasons that are not well elucidated, circulating leukocytes are recruited into the tissues mainly in small vessels such as capillaries and venules. Because ELR ؉ CXC chemokines are important mediators of endothelial-leukocyte interaction, we compared chemokine expression by microvascular and aortic endothelium to investigate whether differences in chemokine expression by various endothelial types could, at least partially, explain the microvascular localization of endothelial-leukocyte interaction. Both in vitro and in vivo models indicate that ELR ؉ CXC chemokine expression is higher in microvascular endothelium than in aortic endothelial cells. These differences can be explained on the basis of the preferential activation of endothelial chemokine production by low intensity shear stress. Low shear activated endothelial ELR ؉ CXC chemokine production via cell surface heparan sulfates, ␤ 3 -integrins, focal adhesion kinase, the mitogen-activated protein kinase p38␤, mitogen-and stress-associated protein kinase-1, and the transcription factor.

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Fluid shear stress inhibits TNF-α activation of JNK but not ERK1/2 or p38 in human umbilical vein endothelial cells: Inhibitory crosstalk among MAPK family members

Cited by 209 publications

References 39 publications

Distinctive role of integrin-mediated adhesion in TNF-induced PKB/Akt and NF-κB activation and endothelial cell survival

Distinctive role of integrin-mediated adhesion in TNF-induced PKB/Akt and NF-κB activation and endothelial cell survival

Shear Flow Attenuates Serum-induced STAT3 Activation in Endothelial Cells

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

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