Human ACE2 Stable Cell Line - A549

Severe acute respiratory syndrome coronavirus (SARS-CoV) is a high-risk infectious agent. The researchers aimed to explore the mechanism by which severe acute respiratory syndrome coronavirus (SARS-CoV) regulates its receptor angiotensin-converting enzyme 2 (ACE2). Studies have found that the spike protein of SARS-CoV (SARS-S) can induce TNF-α converting enzyme (TACE)-dependent stripping of the ACE2 ectodomain. Regulation of TACE activity by SARS-S is dependent on the cytoplasmic domain of ACE2, as deletion mutants lacking the carboxyl-terminal region of ACE2 do not induce ACE2 stripping or TNF-α production. In contrast, the spike protein of HNL63-CoV (NL63-S), which uses ACE2 as a receptor and primarily induces the common cold, did not elicit these cellular responses. Interestingly, analysis of SARS-CoV mRNA expression by real-time RT-PCR revealed that deletion of the cytoplasmic tail of ACE2 or knockdown of TACE expression by siRNA significantly attenuated viral infection. These data show that the cell signals caused by the interaction of SARS-COV and ACE2 actively participate in virus invasion but cause tissue damage. These findings may provide clues to the development of anti-SARS-COV drugs.

Figure 1. In the experiment, the researchers used HEK293T cells expressing ACE2. HEK293T cells were prepared by co-transfection of HIV-1-based lentiviral DNA and plasmids encoding full-length SARS-S or NL63-S. The p24 content of gag protein was measured by using the Retro-Tek HIV-1 p24 ELISA Kit. HEK293T cells expressing ACE2 were infected with SARS-S at a concentration of 100 ng/ml p24. (Haga S, et al., 2008)

Using the Human ACE2 Stable Cell Line provided by Creative Biogene can improve experimental efficiency and stability, eliminating the need to transfect and confirm expression of ACE2 in every experiment, saving time and costs. Since the cell line already expresses ACE2, it can be directly used to study ACE2 cleavage and related mechanisms, simplifying the experimental process.