Rapid CommunicationSera From Patients With Diabetes Do Not Alter the Effect of Mammalian Target of Rapamycin Inhibition on Smooth Muscle Cell ProliferationMoss, Stephanie C MS*; Lightell, Daniel Jr BS*; Deichmann, Richard E Jr MD*; Woods, T Cooper PhD*†Author Information From the *Ochsner Clinic Foundation, New Orleans, LA; and †Department of Pharmacology, Louisiana State University Health Sciences Center-New Orleans, New Orleans, LA. Received for publication October 17, 2008; accepted November 18, 2008. This work was supported by grant numbers 0665320B and 0855316E from the Greater Southeast Affiliate of the American Heart Association and P20RR018766-06 from the National Center for Research Resources, a component of the National Institutes of Health to T.C.W. The authors report no conflicts of interest. Reprints: T. Cooper Woods, PhD, Laboratory of Molecular Cardiology, Basic Science Research, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121 (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: January 2009 - Volume 53 - Issue 1 - p 86-89 doi: 10.1097/FJC.0b013e318195b588 Buy Metrics Abstract Clinical studies of drug-eluting stents delivering the mammalian target of rapamycin (mTOR) inhibitor, rapamycin (Sirolimus), have demonstrated a reduced efficacy for these devices in patients with diabetes, which suggests that the mTOR pathway may cease to be dominant in mediating the vascular response to injury under diabetic conditions. We hypothesized that changes in serum composition accompanying diabetes may reduce the role of mTOR in mediating the vascular response to injury. We measured the ability of a median dose of rapamycin (10 nM) to inhibit the proliferation of human coronary artery smooth muscle cells (huCASMCs) stimulated with serum obtained from donors with diabetes (n = 14) and without diabetes (n = 16). In an additional analysis, we compared the effects of rapamycin on huCASMCs stimulated with the serum of donors with metabolic syndrome (n = 15) versus those without (n = 7). There was no difference in the effect of rapamycin on huCASMC proliferation after stimulation with serum from either donors with diabetes or donors with metabolic syndrome compared with the respective controls. We conclude that the changes in the serum composition common to diabetes and metabolic syndrome are insufficient to diminish the role of mTOR in the progression of cardiovascular disease. © 2009 Lippincott Williams & Wilkins, Inc.