| First Author | Liu F | Year | 2018 |
| Journal | Nat Commun | Volume | 9 |
| Issue | 1 | Pages | 4295 |
| PubMed ID | 30327467 | Mgi Jnum | J:267961 |
| Mgi Id | MGI:6267950 | Doi | 10.1038/s41467-018-06836-4 |
| Citation | Liu F, et al. (2018) MicroRNA-27a controls the intracellular survival of Mycobacterium tuberculosis by regulating calcium-associated autophagy. Nat Commun 9(1):4295 |
| abstractText | Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) kills millions every year, and there is urgent need to develop novel anti-TB agents due to the fast-growing of drug-resistant TB. Although autophagy regulates the intracellular survival of Mtb, the role of calcium (Ca(2+)) signaling in modulating autophagy during Mtb infection remains largely unknown. Here, we show that microRNA miR-27a is abundantly expressed in active TB patients, Mtb-infected mice and macrophages. The target of miR-27a is the ER-located Ca(2+) transporter CACNA2D3. Targeting of this transporter leads to the downregulation of Ca(2+) signaling, thus inhibiting autophagosome formation and promoting the intracellular survival of Mtb. Mice lacking of miR-27a and mice treated with an antagomir to miR-27a are more resistant to Mtb infection. Our findings reveal a strategy for Mtb to increase intracellular survival by manipulating the Ca(2+)-associated autophagy, and may also support the development of host-directed anti-TB therapeutic approaches. |
