3.4.17.23 down angiotensin II downregulates ACE2, but increases the expression of vascular endothelial growth factor and type receptor AT1-R, overview 710171 3.4.17.23 down central angiotensin II type 1 receptors reduce ACE2 expression/activity in hypertensive mice 708683 3.4.17.23 down infection with highly pathogenic avian influenza A H5N1 virus results in downregulation of angiotensin-converting enzyme 2 (ACE2) expression in the lung 732569 3.4.17.23 down mechanisms exist by which SARS-CoV-2 induces shedding of ACE2, together with downregulation of ACE2 gene expression 763771 3.4.17.23 down mice infected with influenza H7N9 virus downregulate ACE2 protein markedly on day 3 after infection 732911 3.4.17.23 down miR-421 (miRNA) downregulates the expression of ACE2 in human cells by interacting with a specific sequence in its 3'-UTR and thereby repressing translation 731675 3.4.17.23 down SARS-CoV downregulates ACE2 protein by binding its spike protein, contributing to severe lung injury 753431 3.4.17.23 down treatment of A-549 lung epithelial cells with 17-beta-estradiol reduces the cellular mRNA levels of ACE2 and TMPRSS2 mRNA, while not affecting FURIN expression 764554 3.4.17.23 additional information ACE2 mRNA and protein expression in murine lung, heart and aorta is not influenced by ibuprofen 764930 3.4.17.23 additional information presence of ibuprofen, flurbiprofen, etoricoxib or paracetamol have no effect on ACE2 mRNA/protein expression and activity in the Caco-2 cell model 764930 3.4.17.23 additional information renal ACE and ACE2 activities increase at 1 year in males, while there are no changes throughout development in females. Renal ACE and ACE2 mRNA and protein show no sex differences but increase by 1 year of age 755365 3.4.17.23 up angiotensin peptides modulate the expression of angiotensin converting enzyme II in the cardiovascular system, angiotensin II upregulates ACE2, modulated through activation of Ang II type 1 receptor, AT1R, and increases Ang-(1-7) formation from Ang II, and ACE2 expression is further enhanced by Ang-(1-7) in a positive feedback loop, molecular mechanism, overview. The upregulation is inhibited by Ang-(1-7) Mas receptor blockade through PD98059 710214 3.4.17.23 up elevated expression in kidney and heart in a rat model with chronic heart failure 731092 3.4.17.23 up expression of ACE2 increases during aging in human lungs. ACE2 expression increases upon telomere shortening or dysfunction in cultured mammalian cells. This increase is controlled at the transcriptional level, and ACE2 promoter activity is DNA damage response-dependent 764575 3.4.17.23 up expression of ACE2 increases during aging in lungs. ACE2 expression increases upon telomere shortening or dysfunction. This increase is controlled at the transcriptional level, and ACE2 promoter activity is DNA damage response-dependent 764575 3.4.17.23 up high sucrose intake induces ACE2 expression in epididymal adipose tissue and kidney, leading to increased ACE2 and angiotensin-(1-7) levels in the adipose tissue 710532 3.4.17.23 up in lung tissues collected from mice that were sub-chronically exposed to air or 0.8 ppm ozone for three weeks, the ACE2 transcripts are significantly elevated in the parenchyma, but not in the extrapulmonary airways and alveolar macrophages. A significant proportion of additional known SARS-CoV-2 host susceptibility genes are upregulated in alveolar macrophages and parenchyma from ozone-exposed mice 765794 3.4.17.23 up infection with highly pathogenic avian influenza A H5N1 virus results in increased expression of angiotensin-converting enzyme 2 (ACE2) in serum 732569 3.4.17.23 up knockdown of TRIM28 induces enzyme (ACE2) expression. TRIM28 knockdown enhances interferon-gamma (IFN-gamma)-induced ACE2 expression through a mechanism involving upregulating IFN-gamma receptor 2 (IFNGR2) in both A549 and PAEpiCs. The upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells is partially reversed by dexamethasone in A-549 cells. TRIM28 is a novel regulator of ACE2 expression and SARS-CoV-2 cell entry 762896 3.4.17.23 up SARS-CoV-2 may bind and activate TLR4 to increase ACE2 expression, facilitating entry and causing hyperinflammation 763421 3.4.17.23 up the enzyme expression is upregulated in case of induced liver fibrosis and is further upregulated by additional administration of ACE I inhibitor peptide, pGlu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, in hepatic stellate cells 708195 3.4.17.23 up TP53 mutant pigs exhibit a sex-specific patho-phenotype due to altered regulation of numerous X chromosome genes. The effect of p53 deficiency on ACE2 expression in pigs is explored. The p53 binding site in the ACE2 promoter is identified and its regulatory effect on ACE2 expression is demonstrated by luciferase assay in porcine primary kidney fibroblast cells. Quantitative PCR and western blot shows tissue- and gender-specific expression changes of ACE2 and its truncated isoform in p53-deficient pigs. mRNA expression of ACE2 is higher in female than male wild-type pigs, with the highest levels in the kidney and small intestine. However, the ACE2 protein expression in the kidney and small intestine is higher in wild-type males. This discrepancy can be explained by the posttranslational ACE2 modifications. In flTP53(R167H) females, the expression of the full-length ACE2 isoform is higher than in wild-type females in most tissues, particularly in small intestine and kidney. In flTP53R167H males, the expression of ACE2 is higher in heart, kidney and lower in small intestine than in wild-type males 762703 3.4.17.23 up up-regulated expression in patients with heart failure and hypertension 732780