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- W2125103246 abstract "Inflammatory migration of immune cells is involved in many human diseases. Identification of molecular pathways and modulators controlling inflammatory migration could lead to therapeutic strategies for treating human inflammation-associated diseases. The role of cannabinoid receptor type 2 (Cnr2) in regulating immune function had been widely investigated, but the mechanism is not fully understood. Through a chemical genetic screen using a zebrafish model for leukocyte migration, we found that both an agonist of the Cnr2 and inhibitor of the 5-lipoxygenase (Alox5, encoded by alox5) inhibit leukocyte migration in response to acute injury. These agents have a similar effect on migration of human myeloid cells. Consistent with these results, we found that inactivation of Cnr2 by zinc finger nuclease-mediated mutagenesis enhances leukocyte migration, while inactivation of Alox5 blocks leukocyte migration. Further investigation indicates that there is a signaling link between Cnr2 and Alox5 and that alox5 is a target of c-Jun. Cnr2 activation down-regulates alox5 expression by suppressing the JNK/c-Jun activation. These studies demonstrate that Cnr2, JNK, and Alox5 constitute a pathway regulating leukocyte migration. The cooperative effect between the Cnr2 agonist and Alox5 inhibitor also provides a potential therapeutic strategy for treating human inflammation-associated diseases. Inflammatory migration of immune cells is involved in many human diseases. Identification of molecular pathways and modulators controlling inflammatory migration could lead to therapeutic strategies for treating human inflammation-associated diseases. The role of cannabinoid receptor type 2 (Cnr2) in regulating immune function had been widely investigated, but the mechanism is not fully understood. Through a chemical genetic screen using a zebrafish model for leukocyte migration, we found that both an agonist of the Cnr2 and inhibitor of the 5-lipoxygenase (Alox5, encoded by alox5) inhibit leukocyte migration in response to acute injury. These agents have a similar effect on migration of human myeloid cells. Consistent with these results, we found that inactivation of Cnr2 by zinc finger nuclease-mediated mutagenesis enhances leukocyte migration, while inactivation of Alox5 blocks leukocyte migration. Further investigation indicates that there is a signaling link between Cnr2 and Alox5 and that alox5 is a target of c-Jun. Cnr2 activation down-regulates alox5 expression by suppressing the JNK/c-Jun activation. These studies demonstrate that Cnr2, JNK, and Alox5 constitute a pathway regulating leukocyte migration. The cooperative effect between the Cnr2 agonist and Alox5 inhibitor also provides a potential therapeutic strategy for treating human inflammation-associated diseases." @default.
- W2125103246 created "2016-06-24" @default.
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- W2125103246 date "2013-05-01" @default.
- W2125103246 modified "2023-10-14" @default.
- W2125103246 title "Cannabinoid Receptor 2 Suppresses Leukocyte Inflammatory Migration by Modulating the JNK/c-Jun/Alox5 Pathway" @default.
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- W2125103246 cites W1901579144 @default.
- W2125103246 cites W1974642601 @default.
- W2125103246 cites W1977715122 @default.
- W2125103246 cites W1978686613 @default.
- W2125103246 cites W1981956565 @default.
- W2125103246 cites W1986305114 @default.
- W2125103246 cites W1987558337 @default.
- W2125103246 cites W1990233945 @default.
- W2125103246 cites W1993564413 @default.
- W2125103246 cites W1994279105 @default.
- W2125103246 cites W2006605504 @default.
- W2125103246 cites W2011363498 @default.
- W2125103246 cites W2012368071 @default.
- W2125103246 cites W2017876495 @default.
- W2125103246 cites W2020179710 @default.
- W2125103246 cites W2021595399 @default.
- W2125103246 cites W2031832859 @default.
- W2125103246 cites W2036052195 @default.
- W2125103246 cites W2044736005 @default.
- W2125103246 cites W2047581866 @default.
- W2125103246 cites W2047642636 @default.
- W2125103246 cites W2048854261 @default.
- W2125103246 cites W2050320031 @default.
- W2125103246 cites W2050376918 @default.
- W2125103246 cites W2056943042 @default.
- W2125103246 cites W2058177171 @default.
- W2125103246 cites W2058955046 @default.
- W2125103246 cites W2060589571 @default.
- W2125103246 cites W2062144273 @default.
- W2125103246 cites W2063155826 @default.
- W2125103246 cites W2066897722 @default.
- W2125103246 cites W2072441201 @default.
- W2125103246 cites W2074171762 @default.
- W2125103246 cites W2075224548 @default.
- W2125103246 cites W2075894678 @default.
- W2125103246 cites W2081084728 @default.
- W2125103246 cites W2086145996 @default.
- W2125103246 cites W2087935405 @default.
- W2125103246 cites W2100340759 @default.
- W2125103246 cites W2102421593 @default.
- W2125103246 cites W2102456349 @default.
- W2125103246 cites W2103381667 @default.
- W2125103246 cites W2103826070 @default.
- W2125103246 cites W2104785885 @default.
- W2125103246 cites W2118305000 @default.
- W2125103246 cites W2119417389 @default.
- W2125103246 cites W2122682542 @default.
- W2125103246 cites W2130069008 @default.
- W2125103246 cites W2130848106 @default.
- W2125103246 cites W2135314437 @default.
- W2125103246 cites W2142488420 @default.
- W2125103246 cites W2143424812 @default.
- W2125103246 cites W2146669471 @default.
- W2125103246 cites W2146965545 @default.
- W2125103246 cites W2147244574 @default.
- W2125103246 cites W2148194748 @default.
- W2125103246 cites W2159876689 @default.
- W2125103246 cites W2162859509 @default.
- W2125103246 cites W2166962970 @default.
- W2125103246 cites W2170049370 @default.
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- W2125103246 doi "https://doi.org/10.1074/jbc.m113.453811" @default.
- W2125103246 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3650391" @default.
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