<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>72(4)</volume><submitter>Matsuo H</submitter><pubmed_abstract>Hypertension and atherosclerosis are often found in one patient causing serious cardiovascular events. An animal model simultaneously expressing hypertension and atherosclerosis would be useful to study such a complex risk status. We therefore attempted to introduce a null mutation of the apolipoprotein E (ApoE) gene into the spontaneously hypertensive rat (SHR) using CRISPR/Cas9 to establish a genetic model for atherosclerosis with hypertension. We successfully established SHR&lt;sup>ApoE(-/-)&lt;/sup> having a 13-bps deletion in the 5'-end of ApoE gene. Deletion of ApoE protein was confirmed by Western blotting. Blood pressure of SHR&lt;sup>ApoE(-/-)&lt;/sup> was comparable to that of SHR. Feeding the rats with high fat high cholesterol diet (HFD) caused a significant increase in LDL cholesterol as </pubmed_abstract><journal>Experimental animals</journal><pagination>439-445</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10658095</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Apolipoprotein E-depletion accelerates arterial fat deposition in the spontaneously hypertensive rat.</pubmed_title><pmcid>PMC10658095</pmcid><pubmed_authors>Mashimo T</pubmed_authors><pubmed_authors>Matsuo H</pubmed_authors><pubmed_authors>Kawakami K</pubmed_authors><pubmed_authors>Yamada T</pubmed_authors><pubmed_authors>Nabika T</pubmed_authors><pubmed_authors>Kaneko T</pubmed_authors><pubmed_authors>Ohara H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Apolipoprotein E-depletion accelerates arterial fat deposition in the spontaneously hypertensive rat.</name><description>Hypertension and atherosclerosis are often found in one patient causing serious cardiovascular events. An animal model simultaneously expressing hypertension and atherosclerosis would be useful to study such a complex risk status. We therefore attempted to introduce a null mutation of the apolipoprotein E (ApoE) gene into the spontaneously hypertensive rat (SHR) using CRISPR/Cas9 to establish a genetic model for atherosclerosis with hypertension. We successfully established SHR&lt;sup>ApoE(-/-)&lt;/sup> having a 13-bps deletion in the 5'-end of ApoE gene. Deletion of ApoE protein was confirmed by Western blotting. Blood pressure of SHR&lt;sup>ApoE(-/-)&lt;/sup> was comparable to that of SHR. Feeding the rats with high fat high cholesterol diet (HFD) caused a significant increase in LDL cholesterol as </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2025-04-04T12:18:11.459Z</modification><creation>2025-04-04T12:18:11.459Z</creation></dates><accession>S-EPMC10658095</accession><cross_references><pubmed>37081644</pubmed><doi>10.1538/expanim.23-0012</doi></cross_references></HashMap>