Hydroxysteroid sulfotransferase (SULT2A) catalyzes the transfer of sulfate from the physiological sulfate donor 3′‐phosphoadenosine‐5′‐phosphosulfate (PAPS) to endogenous and xenobiotic substrates. In human hepatocytes, PAPS synthesis is catalyzed by PAPS synthase 2 (PAPSS2). HepG2 cells were stably transduced with lentivirus expressing either non‐targeting small interfering RNA (siRNA) (siNT‐HepG2) or siRNA directed against PAPS synthase 2 (siPAPSS2‐HepG2). Relative to siNT‐HepG2, siPAPSS2‐HepG2 cells transiently transfected with a reporter plasmid containing 1.5 kb of a murine SULT2A 5′‐flanking region demonstrated a significant (~2‐fold) increase in reporter expression. Disruption of a putative LXR motif in the murine SULT2A 5′‐flanking region suppressed the induction of SULT2A reporter expression produced by PAPSS2 knock‐down. Real‐time RT‐PCR analysis also demonstrated ~3‐fold induction of endogenous human SULT2A1 mRNA expression by PAPSS2 knock‐down. These results indicate that both human and murine SULT2A transcription are up‐regulated in response to PAPSS2 knock‐down, and implicate a role for LXR as a sulfate sensor. Supported by ES058223 (M.R.M.), HL50710 (T.A.K) and ES06636.
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