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Intracerebroventricular (icv) injection of replication‐deficient adenovirus encoding Cre‐recombinase (Ad‐Cre) reduces estrogen receptor alpha (ERα) staining in the subfornical organ of ERα flox female mice
Author(s) -
Xue Baojian,
BadauePassos Daniel,
Beltz Terry G,
Johnson Ralph F,
Johnson Alan Kim,
Hay Meredith
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.941.9
Subject(s) - cre recombinase , estrogen receptor , biology , estrogen receptor alpha , microbiology and biotechnology , subfornical organ , endocrinology , transgene , genetically modified mouse , medicine , receptor , angiotensin ii , gene , genetics , cancer , breast cancer
The estrogen receptor knock out mouse (ERKO) has been used in our early studies that implicate ER involvement in protecting females from angiotensin II (ANG II)‐dependent hypertension. However, the relative role of peripheral vs central ER in this effect remains uncertain. This is mainly because of the difficulties in experimentally dissecting this complex system where different forms of ER (i.e., ERα and ERβ) are expressed in numerous sites and cell types both in the brain and in the periphery. In the present study, a ¡°floxed¡± ERα transgenic mouse line harboring a loxP‐flanked (exon II) for the ERα (ERα flox ) was used to create an animal model in which it is possible to knock down one specific ER subtype (i.e., ERα) in a targeted body structure/region. Ad‐Cre or a control empty vector (Ad‐Con) was injected into the lateral ventricle (2 μl) in ER α flox female mice. Ten days later, coronal brain sections were double immunostained for ERα and Cre‐recombinase. Cre‐treated ER α flox mice showed reduced ERα staining in the subfornical organ (SFO) along with intense Cre staining at this site. These results indicate that using the Cre recombinase/loxP system in combination with viral gene transfer of Cre, conditional gene deletion can be achieved in the SFO and other cardiovascular regulatory sites in the CNS. This will allow us to assess the role of central ER subtypes in ANG II‐induced hypertension. (Support: NIH HL‐59676 and HL‐62261)