The Role of CD147 in Pathological Cardiac Hypertrophy Is Regulated by Glycosylation

Figure 3

Glycosylation site mutations mitigated the prohypertrophic effects of CD147. (a) Representative images of the hearts and HE staining of four-chamber view sections. (b) Representative images of CMR examinations, HE staining, and WGA staining of heart sections from the indicated groups. (c) Statistical results for HW/BW, HW/TL, LW/TL, and myocyte cross-sectional areas for the indicated groups ( mice/group). (d) Western blot analysis of ANP and β-MHC in murine hearts from the indicated groups 8 weeks after transverse aortic constriction (TAC) surgery ( mice/group). Upper panel, representative blots. Lower panel, quantitative results. (e) mRNA levels of Anp, Bnp, α-Mhc, and β-Mhc in the indicated groups ( mice/group). Results were normalised to Gapdh levels and converted to fold induction relative to the sham group. vs. the sham group; vs. the sham group; vs. the sham group; vs. the sham group; ^# vs. the vehicle group; ^## vs. the vehicle group; ^### vs. the vehicle group; ^✟ vs. the OE group; ^✟✟ vs. the OE group; ^✟✟✟ vs. the OE group. CMR: cardiovascular magnetic resonance; HE: haematoxylin-eosin; WGA: wheat germ agglutinin; HW: heart weight; BW: body weight; LW: lung weight; TL: tibia length; ANP: atrial natriuretic peptide; BNP: brain natriuretic peptide; β-MHC: myosin heavy chain β; α-MHC: myosin heavy chain α.

(a)

(b)

(c)

(d)

(e)