Inactivation of Mxi1 induces Il-8 secretion activation in polycystic kidney

Kyung Hyun Yoo; Young Hoon Sung; Moon Hee Yang; Jeong Ok Jeon; Yeon Joo Yook; Yu Mi Woo; Han Woong Lee; Jong Hoon Park

doi:10.1016/j.bbrc.2007.02.103

Inactivation of Mxi1 induces Il-8 secretion activation in polycystic kidney

Kyung Hyun Yoo, Young Hoon Sung, Moon Hee Yang, Jeong Ok Jeon, Yeon Joo Yook, Yu Mi Woo, Han Woong Lee, Jong Hoon Park

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

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Abstract

The Mxi1 proteins are biochemical and biological antagonists of c-myc oncoprotein. It has been reported that the overexpression pattern of c-myc might be similar to a molecular feature of early and late stages of human autosomal dominant polycystic kidney disease. We identified the cyst phenotype in Mxi1-deficient mice aged 6-12 months using H&E staining. Some chemokines containing a protein domain similar to human IL-8, which is associated with the inflammatory response, were subsequently selected from the up-regulated genes. We confirmed the expression level of these chemokines and measured protein concentrations of IL-8 using ELISA in the Mxi1-knockdown cells. IL-8 was found to be significantly increased in Mxi1-knockdown cells. We found that p38 MAP kinase activation was involved in the signal transduction of the Mxi1-inactivated secretion of IL-8. Therefore, we could suggest that the inactivation of Mxi1 leads to the inflammatory response and has the potential to induce polycystic renal disease.

Original language	English
Pages (from-to)	85-90
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	356
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2007.02.103
Publication status	Published - 2007 Apr 27

Bibliographical note

Funding Information:
This work was supported by the Korea Science and Engineering Foundation (KOSEF) through the National Research Lab. Program funded by the Ministry of Science and Technology (M10500000101-06J0000-10110), KOSEF grant funded by the Korea government (MOST) (ROI-2004-000-10182-0), Grants from 21C Frontier FHGP (FG05-22-02) and the BRC Frontier (M103KV010018-05K2201-01830). We are grateful to Dr. J.Y. Noh at Sookmyng Women’s University for discussions.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2007.02.103

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title = "Inactivation of Mxi1 induces Il-8 secretion activation in polycystic kidney",

abstract = "The Mxi1 proteins are biochemical and biological antagonists of c-myc oncoprotein. It has been reported that the overexpression pattern of c-myc might be similar to a molecular feature of early and late stages of human autosomal dominant polycystic kidney disease. We identified the cyst phenotype in Mxi1-deficient mice aged 6-12 months using H&E staining. Some chemokines containing a protein domain similar to human IL-8, which is associated with the inflammatory response, were subsequently selected from the up-regulated genes. We confirmed the expression level of these chemokines and measured protein concentrations of IL-8 using ELISA in the Mxi1-knockdown cells. IL-8 was found to be significantly increased in Mxi1-knockdown cells. We found that p38 MAP kinase activation was involved in the signal transduction of the Mxi1-inactivated secretion of IL-8. Therefore, we could suggest that the inactivation of Mxi1 leads to the inflammatory response and has the potential to induce polycystic renal disease.",

author = "Yoo, {Kyung Hyun} and Sung, {Young Hoon} and Yang, {Moon Hee} and Jeon, {Jeong Ok} and Yook, {Yeon Joo} and Woo, {Yu Mi} and Lee, {Han Woong} and Park, {Jong Hoon}",

note = "Funding Information: This work was supported by the Korea Science and Engineering Foundation (KOSEF) through the National Research Lab. Program funded by the Ministry of Science and Technology (M10500000101-06J0000-10110), KOSEF grant funded by the Korea government (MOST) (ROI-2004-000-10182-0), Grants from 21C Frontier FHGP (FG05-22-02) and the BRC Frontier (M103KV010018-05K2201-01830). We are grateful to Dr. J.Y. Noh at Sookmyng Women{\textquoteright}s University for discussions.",

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AU - Woo, Yu Mi

AU - Lee, Han Woong

AU - Park, Jong Hoon

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N2 - The Mxi1 proteins are biochemical and biological antagonists of c-myc oncoprotein. It has been reported that the overexpression pattern of c-myc might be similar to a molecular feature of early and late stages of human autosomal dominant polycystic kidney disease. We identified the cyst phenotype in Mxi1-deficient mice aged 6-12 months using H&E staining. Some chemokines containing a protein domain similar to human IL-8, which is associated with the inflammatory response, were subsequently selected from the up-regulated genes. We confirmed the expression level of these chemokines and measured protein concentrations of IL-8 using ELISA in the Mxi1-knockdown cells. IL-8 was found to be significantly increased in Mxi1-knockdown cells. We found that p38 MAP kinase activation was involved in the signal transduction of the Mxi1-inactivated secretion of IL-8. Therefore, we could suggest that the inactivation of Mxi1 leads to the inflammatory response and has the potential to induce polycystic renal disease.

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Inactivation of Mxi1 induces Il-8 secretion activation in polycystic kidney

Abstract

Bibliographical note

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