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. 2021 Nov 8;6(21):e148749. doi: 10.1172/jci.insight.148749

Figure 1. CHI3L1 stimulates pulmonary ACE2 and SPP.

Figure 1

Eight-week-old WT (–) and CHI3L1 Tg (+) mice were sacrificed after 2 weeks of transgene induction with doxycycline. Levels of Ace2 and SPP mRNA and protein in lungs from WT and CHI3L1 Tg mice were evaluated using lung lysates and paraffin tissue blocks. (A) Comparisons of expression levels of ACE2 and SPP in lungs from WT (Tg–) and CHI3L1 Tg+ mice using semiquantitative real-time reverse transcription PCR (RT-qPCR) indexed to β-actin controls. (B) Western immunoblot comparisons of ACE2 and SPP levels in lungs from WT (Tg–) and CHI3L1 Tg+ mice. (C and D) IHC of ACE2, CTSL, and TMPRSS2 in lungs from WT and CHI3L1 Tg mice. (E) Double-label IHC comparing localization of ACE2, TMPRSS2, and CD31 in lungs from CHI3L1 Tg mice. Arrows on C–E indicate stain+ cells. Each value in A is from a different animal; mean ± SEM is illustrated. B–E are representative of at least 3 separate evaluations. β-Actin was used as an internal control. ACE2, murine angiotensin converting enzyme 2; TMPRSS2, transmembrane serine protease 2; CTSL, Cathepsin L. Scale bars: 100 μm. *P < 0.05 (Student t test).