LPP Expression During In Vitro Smooth Muscle Differentiation and Stent-Induced Vascular Injury
- 17 February 2006
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Circulation Research
- Vol. 98 (3), 378-385
- https://doi.org/10.1161/01.res.0000202802.34727.fd
Abstract
Lipoma preferred partner (LPP) has been identified as a protein highly expressed in smooth muscle (SM) tissues. The aim of the present study was to determine mechanisms that regulate LPP expression in an in vitro model of SM cell (SMC) differentiation and in stent-induced pig coronary vessel injury. All trans-retinoic acid treatment of A404 cells induced a strong increase in LPP, as well as SM α-actin, SM myosin heavy chain, and smoothelin mRNA levels, in a Rho kinase (ROK)-dependent manner. Adenovirus mediated overexpression of myocardin in A404 cells significantly increased LPP mRNA expression. Interestingly, inactivation of RhoA with C3-exoenzyme or treatment with ROK inhibitors strongly inhibited myocardin mRNA expression in retinoic acid–treated A404 cells or human iliac vein SMCs. LPP silencing with short interfering RNA significantly decreased SMC migration. LPP expression was also markedly decreased in focal adhesion kinase (FAK)-null cells known to have impaired migration but rescued with inducible expression of FAK. LPP expression in FAK-null fibroblasts enhanced cell spreading. In stented pig coronary vessels, LPP was expressed in the neointima of cells lacking smoothelin and showed expression patterns identical to those of SM α-actin. In conclusion, LPP appears to be a myocardin-, RhoA/ROK-dependent SMC differentiation marker that plays a role in regulating SMC migration.Keywords
This publication has 32 references indexed in Scilit:
- L-type Voltage-Gated Ca 2+ Channels Modulate Expression of Smooth Muscle Differentiation Marker Genes via a Rho Kinase/Myocardin/SRF–Dependent MechanismCirculation Research, 2004
- Myocardin and Prx1 Contribute to Angiotensin II-Induced Expression of Smooth Muscle α-ActinCirculation Research, 2004
- Prediction of Cell Type-Specific Gene Modules: Identification and Initial Characterization of a Core Set of Smooth Muscle-Specific GenesGenome Research, 2003
- Myocardin Is a Key Regulator of CArG-Dependent Transcription of Multiple Smooth Muscle Marker GenesCirculation Research, 2003
- Actin Dynamics Control SRF Activity by Regulation of Its Coactivator MALCell, 2003
- FAK induces expression of Prx1 to promote tenascin-C–dependent fibroblast migrationThe Journal of cell biology, 2003
- Rho kinase and matrix metalloproteinase inhibitors cooperate to inhibit angiogenesis and growth of human prostate cancer xenotransplantsThe FASEB Journal, 2002
- Spatial Control of Actin Filament AssemblyCell, 1998
- Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient miceNature, 1995
- Dense bodies and actin polarity in vertebrate smooth muscle.The Journal of cell biology, 1982