Syndecan-4 promotes the retention of phosphatidylinositol 4,5-bisphosphate in the plasma membrane

Soojin Kwon; Hyowon Son; Youngsil Choi; Jung hyun Lee; Sojoong Choi; Yangmi Lim; Inn Oc Han; Eok Soo Oh

doi:10.1016/j.febslet.2009.06.039

Syndecan-4 promotes the retention of phosphatidylinositol 4,5-bisphosphate in the plasma membrane

Soojin Kwon, Hyowon Son, Youngsil Choi, Jung hyun Lee, Sojoong Choi, Yangmi Lim, Inn Oc Han, Eok Soo Oh

Department of Life Science

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

4 Scopus citations

Abstract

Although phosphatidylinositol 4,5-bisphosphate (PIP₂) regulates syndecan-4 function, the potential influence of syndecan-4 on PIP₂ remains unknown. GFP containing PIP₂-binding-PH domain of phospholipase Cδ (GFP-PHδ) was used to monitor PIP₂. Syndecan-4 overexpression in COS-7 cells enhanced membrane translocation of GFP-PHδ, while the opposite was observed when syndecan-4 was knocked-down. PIP₂ levels were higher in total phospholipids extracted from rat embryo fibroblasts expressing syndecan-4. Syndecan-4-induced membrane targeting of GFP-PHδ was further enhanced by phosphoinositide-3-kinase inhibitor, but not by phospholipase C (PLC) inhibitor. Besides, both ionomycin and epidermal growth factor caused dissociation of GFP-PHδ from plasma membrane, an effect that was significantly delayed by syndecan-4 over-expression. Collectively, these data suggest that syndecan-4 promotes plasma membrane retention of PIP₂ by negatively regulating PLC-dependent PIP₂ degradation.

Original language	English
Pages (from-to)	2395-2400
Number of pages	6
Journal	FEBS Letters
Volume	583
Issue number	14
DOIs	https://doi.org/10.1016/j.febslet.2009.06.039
State	Published - 21 Jul 2009

Bibliographical note

Funding Information:
This research was supported by Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2009-0071381 to ESO) and in part by Grant No. R15-2006-020 from the NCRC program of the MEST and the KOSEF through the Center for Cell Signaling and Drug Discovery Research at Ewha Womans University.

Keywords

Adhesion
Phosphatidylinositol 4,5-bisphosphate
Signal transduction
Syndecan

Access to Document

10.1016/j.febslet.2009.06.039

Cite this

@article{b1efe09a2b3a46a885158920e5acec65,

title = "Syndecan-4 promotes the retention of phosphatidylinositol 4,5-bisphosphate in the plasma membrane",

abstract = "Although phosphatidylinositol 4,5-bisphosphate (PIP2) regulates syndecan-4 function, the potential influence of syndecan-4 on PIP2 remains unknown. GFP containing PIP2-binding-PH domain of phospholipase Cδ (GFP-PHδ) was used to monitor PIP2. Syndecan-4 overexpression in COS-7 cells enhanced membrane translocation of GFP-PHδ, while the opposite was observed when syndecan-4 was knocked-down. PIP2 levels were higher in total phospholipids extracted from rat embryo fibroblasts expressing syndecan-4. Syndecan-4-induced membrane targeting of GFP-PHδ was further enhanced by phosphoinositide-3-kinase inhibitor, but not by phospholipase C (PLC) inhibitor. Besides, both ionomycin and epidermal growth factor caused dissociation of GFP-PHδ from plasma membrane, an effect that was significantly delayed by syndecan-4 over-expression. Collectively, these data suggest that syndecan-4 promotes plasma membrane retention of PIP2 by negatively regulating PLC-dependent PIP2 degradation.",

keywords = "Adhesion, Phosphatidylinositol 4,5-bisphosphate, Signal transduction, Syndecan",

author = "Soojin Kwon and Hyowon Son and Youngsil Choi and Lee, {Jung hyun} and Sojoong Choi and Yangmi Lim and Han, {Inn Oc} and Oh, {Eok Soo}",

note = "Funding Information: This research was supported by Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2009-0071381 to ESO) and in part by Grant No. R15-2006-020 from the NCRC program of the MEST and the KOSEF through the Center for Cell Signaling and Drug Discovery Research at Ewha Womans University.",

year = "2009",

month = jul,

day = "21",

doi = "10.1016/j.febslet.2009.06.039",

language = "English",

volume = "583",

pages = "2395--2400",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Wiley-Blackwell",

number = "14",

}

TY - JOUR

T1 - Syndecan-4 promotes the retention of phosphatidylinositol 4,5-bisphosphate in the plasma membrane

AU - Kwon, Soojin

AU - Son, Hyowon

AU - Choi, Youngsil

AU - Lee, Jung hyun

AU - Choi, Sojoong

AU - Lim, Yangmi

AU - Han, Inn Oc

AU - Oh, Eok Soo

N1 - Funding Information: This research was supported by Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2009-0071381 to ESO) and in part by Grant No. R15-2006-020 from the NCRC program of the MEST and the KOSEF through the Center for Cell Signaling and Drug Discovery Research at Ewha Womans University.

PY - 2009/7/21

Y1 - 2009/7/21

N2 - Although phosphatidylinositol 4,5-bisphosphate (PIP2) regulates syndecan-4 function, the potential influence of syndecan-4 on PIP2 remains unknown. GFP containing PIP2-binding-PH domain of phospholipase Cδ (GFP-PHδ) was used to monitor PIP2. Syndecan-4 overexpression in COS-7 cells enhanced membrane translocation of GFP-PHδ, while the opposite was observed when syndecan-4 was knocked-down. PIP2 levels were higher in total phospholipids extracted from rat embryo fibroblasts expressing syndecan-4. Syndecan-4-induced membrane targeting of GFP-PHδ was further enhanced by phosphoinositide-3-kinase inhibitor, but not by phospholipase C (PLC) inhibitor. Besides, both ionomycin and epidermal growth factor caused dissociation of GFP-PHδ from plasma membrane, an effect that was significantly delayed by syndecan-4 over-expression. Collectively, these data suggest that syndecan-4 promotes plasma membrane retention of PIP2 by negatively regulating PLC-dependent PIP2 degradation.

AB - Although phosphatidylinositol 4,5-bisphosphate (PIP2) regulates syndecan-4 function, the potential influence of syndecan-4 on PIP2 remains unknown. GFP containing PIP2-binding-PH domain of phospholipase Cδ (GFP-PHδ) was used to monitor PIP2. Syndecan-4 overexpression in COS-7 cells enhanced membrane translocation of GFP-PHδ, while the opposite was observed when syndecan-4 was knocked-down. PIP2 levels were higher in total phospholipids extracted from rat embryo fibroblasts expressing syndecan-4. Syndecan-4-induced membrane targeting of GFP-PHδ was further enhanced by phosphoinositide-3-kinase inhibitor, but not by phospholipase C (PLC) inhibitor. Besides, both ionomycin and epidermal growth factor caused dissociation of GFP-PHδ from plasma membrane, an effect that was significantly delayed by syndecan-4 over-expression. Collectively, these data suggest that syndecan-4 promotes plasma membrane retention of PIP2 by negatively regulating PLC-dependent PIP2 degradation.

KW - Adhesion

KW - Phosphatidylinositol 4,5-bisphosphate

KW - Signal transduction

KW - Syndecan

UR - http://www.scopus.com/inward/record.url?scp=67650101214&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2009.06.039

DO - 10.1016/j.febslet.2009.06.039

M3 - Article

C2 - 19560461

AN - SCOPUS:67650101214

SN - 0014-5793

VL - 583

SP - 2395

EP - 2400

JO - FEBS Letters

JF - FEBS Letters

IS - 14

ER -

Syndecan-4 promotes the retention of phosphatidylinositol 4,5-bisphosphate in the plasma membrane

Abstract

Bibliographical note

Keywords

Access to Document

Fingerprint

Cite this