Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca2+/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways

Bei Li; Yuqiang Shi; Jianhong Shu; Junling Gao; Ping Wu; Shao Jun Tang

doi:10.1074/jbc.M112.381046

Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways

Bei Li
, Yuqiang Shi
, Jianhong Shu
, Junling Gao
, Ping Wu
, Shao Jun Tang

Anesthesiology

University of Texas Medical Branch at Galveston
Hainan Provincial Institute for Drug Control
Zhejiang Sci-Tech University

Research output: Contribution to journal › Article › peer-review

55 Scopus citations

Abstract

Background: HIV-1 infection causes chronic neuroinflammation in the central nervous system (CNS). Results: The spinal cytokine up-regulation induced by HIV-1 gp120 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways. Conclusion: gp120 stimulates cytokine expression in the spinal cord dorsal horn by activating Wnt5a signaling. Significance: The finding reveals Wnt signaling-mediated novel mechanisms by which HIV-1 may cause neuroinflammation.

Original language	English
Pages (from-to)	13610-13619
Number of pages	10
Journal	Journal of Biological Chemistry
Volume	288
Issue number	19
DOIs	https://doi.org/10.1074/jbc.M112.381046
State	Published - May 10 2013

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Li, B., Shi, Y., Shu, J., Gao, J., Wu, P., & Tang, S. J. (2013). Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways. Journal of Biological Chemistry, 288(19), 13610-13619. https://doi.org/10.1074/jbc.M112.381046

Li, Bei ; Shi, Yuqiang ; Shu, Jianhong et al. / Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways. In: Journal of Biological Chemistry. 2013 ; Vol. 288, No. 19. pp. 13610-13619.

@article{e22afee5db4c4b4a83d309145f034bd8,

title = "Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca2+/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways",

abstract = "Background: HIV-1 infection causes chronic neuroinflammation in the central nervous system (CNS). Results: The spinal cytokine up-regulation induced by HIV-1 gp120 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways. Conclusion: gp120 stimulates cytokine expression in the spinal cord dorsal horn by activating Wnt5a signaling. Significance: The finding reveals Wnt signaling-mediated novel mechanisms by which HIV-1 may cause neuroinflammation.",

author = "Bei Li and Yuqiang Shi and Jianhong Shu and Junling Gao and Ping Wu and Tang, \{Shao Jun\}",

year = "2013",

month = may,

day = "10",

doi = "10.1074/jbc.M112.381046",

language = "English",

volume = "288",

pages = "13610--13619",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

number = "19",

}

Li, B, Shi, Y, Shu, J, Gao, J, Wu, P & Tang, SJ 2013, 'Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways', Journal of Biological Chemistry, vol. 288, no. 19, pp. 13610-13619. https://doi.org/10.1074/jbc.M112.381046

Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways. / Li, Bei; Shi, Yuqiang; Shu, Jianhong et al.
In: Journal of Biological Chemistry, Vol. 288, No. 19, 10.05.2013, p. 13610-13619.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca2+/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways

AU - Li, Bei

AU - Shi, Yuqiang

AU - Shu, Jianhong

AU - Gao, Junling

AU - Wu, Ping

AU - Tang, Shao Jun

PY - 2013/5/10

Y1 - 2013/5/10

N2 - Background: HIV-1 infection causes chronic neuroinflammation in the central nervous system (CNS). Results: The spinal cytokine up-regulation induced by HIV-1 gp120 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways. Conclusion: gp120 stimulates cytokine expression in the spinal cord dorsal horn by activating Wnt5a signaling. Significance: The finding reveals Wnt signaling-mediated novel mechanisms by which HIV-1 may cause neuroinflammation.

AB - Background: HIV-1 infection causes chronic neuroinflammation in the central nervous system (CNS). Results: The spinal cytokine up-regulation induced by HIV-1 gp120 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways. Conclusion: gp120 stimulates cytokine expression in the spinal cord dorsal horn by activating Wnt5a signaling. Significance: The finding reveals Wnt signaling-mediated novel mechanisms by which HIV-1 may cause neuroinflammation.

UR - https://www.scopus.com/pages/publications/84877721632

U2 - 10.1074/jbc.M112.381046

DO - 10.1074/jbc.M112.381046

M3 - Article

C2 - 23539626

AN - SCOPUS:84877721632

SN - 0021-9258

VL - 288

SP - 13610

EP - 13619

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 19

ER -

Li B, Shi Y, Shu J, Gao J, Wu P, Tang SJ. Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways. Journal of Biological Chemistry. 2013 May 10;288(19):13610-13619. doi: 10.1074/jbc.M112.381046

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