StarD7 deficiency modulates the expression of extracellular matrix associated-proteins in HTR8/SVneo cells

CRUZ DEL PUERTO, MARIANO; MARÍA LAURA ROJAS; FLORES-MARTÍN JÉSICA; GRACIELA PANZETTA DE DUTARI; GENTI DE RAIMONDI SUSANA

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

STARD7 DEFICIENCY MODULATES THE EXPRESSIONOF EXTRACELLULAR MATRIX ASSOCIATED-PROTEINSIN HTR8/SVNEO CELLSMariano Matias Arzud Cruz Del Puerto, María Laura Rojas,Jésica Flores-Martín, Graciela Panzetta- Dutari, SusanaGenti-RaimondiDpto. Bioquímica Clínica, Facultad de Ciencias Químicas-UNC. CIBICI-CONICETStarD7 transcript encodes an intracellular lipid transport protein,a member of the START domain superfamily, which is involved inmany physiological processes. It facilitates the delivery of phosphatidylcholineto the mitochondria and previous results indicated thatStarD7 knockdown decreases ACBG2 multidrug transporter level,cell migration, proliferation, and phospholipid synthesis. Additionally,we reported that its suppression promotes reticulum endoplasmicstress and ROS production. Here, we examined the effect of StarD7silencing on several extracellular matrix (ECM) associated-proteinsin HTR8/SVneo cells derived from human first-trimester. Data fromqPCR, western blot and immunofluorescence analysis demonstrateda significant increase in the mRNA and protein levels of integrinα5 in the HTR8/SVneo cells transfected with StarD7 siRNA comparedto control siRNA. Additionally, a clear increase in the transcriptlevel of integrin β1, as well as in the mature β1 and integrinα1 proteins were detected. Furthermore, StarD7 silencing leads toan increase in β-catenin and nidogen-1 at both protein and mRNAlevels, as well as in the amount of MMP9 secreted to the culture medium.Collectively, our studies indicate that StarD7 depletion causesa dysregulation in several ECM-associated proteins suggesting thatbeyond its role in lipid transport, StarD7 contributes to maintain cellularhomeostasis.