Mitochondrial Ultrastructural Alterations and Declined M2 Receptor Density Were Involved in Cardiac Dysfunction in Rats after Long Term Treatment with Autoantibodies against M2 Muscarinic Receptor
Fig 1
Establishment of M2-AA-positive rat models by actively immunizing with M2AChR-el2 antigen peptides for 18 months.
(A) Time courses of M2-AA production during the process of active immunization in rats. Data are presented as mean ± SEM of optical density (OD) values measured by ELISA from three independent experiments at dilution of 1/640. The M2–AA group (n = 26) was immunized with a mixture of M2AChR-el2 antigen peptides and immunologic adjuvant, the vehicle group (n = 27) was immunized with a mixture of physiological saline and immunologic adjuvant. *P<0.05, **P<0.01 vs. vehicle group at the respective time-point. (B) Observation of the transverse sections of the hearts after 18 months of immunization with M2AChR-el2 antigen peptides. Hearts from the vehicle group showed normal chamber size and wall thickness, while hearts from the M2-AA group showed dilatation of the right ventricle with wall thinning. M2-AA, autoantibodies against M2 muscarinic receptor; M2AChR-el2, the second extracellular loop of M2 muscarinic receptor.