Inhibition of Heme Oxygenase-1 Interferes with the Transforming Activity of the Kaposi Sarcoma Herpesvirusencoded G Protein-coupled Receptor

Neferine inhibits angiotensin II-stimulated proliferation in vascular smooth muscle cells through heme oxygenase-1

“…Conversely, over-expression of HO-1 by either transfection of the HO-1 gene or exogenous administration of a certain HO-1 inducer reduces excessive VSMC proliferation [25] . However, the effect of HO-1 on cell proliferation is highly variable and seems to be cell-type specific [8,[26][27][28] , raising an important question of whether the antiproliferative effect of neferine on VSMC could be mediated via HO-1 expression. To test this, the effects on both HO-1 expression and growth inhibition of neferine were determined with the same concentration of neferine used in the present study.…”

Down-regulation of heme oxygenase-1 by SVCV infection

“…HO-1 has also been shown to interfere hepatitis C virus (HCV) [3e5], hepatitis B virus (HBV) [6] and human immunodeficiency virus (HIV) [7] infections. In addition to the putative antiviral properties against these viruses, the induction of HO-1 may contribute to the pathogenesis of Kaposi's sarcoma (KS), a multifocal angioproliferative disorder following infection with human herpes virus-8 (HH8, also known as Kaposi's sarcoma-associated herpes virus, KSHV) [8].…”

The Gα12/13 Family of Heterotrimeric G Proteins and the Small GTPase RhoA Link the Kaposi Sarcoma-associated Herpes Virus G Protein-coupled Receptor to Heme Oxygenase-1 Expression and Tumorigenesis

“…pCEFL-AU5-vGPCR, pCDNAIII-␤-galactosidase, pCEFL-green fluorescent protein (GFP), pCDNAIII-G␣ 12 QL, pCEFL-HA-G␣ 13 QL, pCDNAIII-G␣ q QL, pCDNAIII-G␣ i QL, pCDNAIII-G␣ s QL, pCEFL-HA-m2, pCEFL-HA-G 13i5 , pCEFL-HA-G qi5 , pCEFL-p115RGS-D, pCEFL-AU5-RhoAQL, pCEFL-HA-HO-1, pCEFL-AU1-PDZRhoGEF, pCEFL-RhoN19, pEF-C3, pCEFL-AU5-Rac1QL, pNFB-Luc, and pSshRNAHO-1 have been already described (25,(37)(38)(39)(40). pCEP4, a plasmid carrying a hygromycin resistance gene, was commercially purchased (Invitrogen).…”

“…NIH-3T3 fibroblasts were maintained in DMEM (Invitrogen) supplemented with 10% calf serum. NIH-vGPCR cells were prepared as described (25). Stable transfection of NIH-3T3 cells was performed using the calcium phosphate technique (40).…”

“…Additionally, inhibition of HO-1 expression or activity critically impairs vGPCRinduced tumorigenesis in allograft tumor animal models (25). Despite the implication of HO-1 as a vGPCR downstream target, the nature of the molecular pathways connecting the receptor to HO-1 expression remains unknown.…”