Additional file 1 of Glycated ACE2 reduces anti-remodeling effects of renin-angiotensin system inhibition in human diabetic hearts
Creators: name: Marfella, Raffaele
name: D’Onofrio, Nunzia
name: Mansueto, Gelsomina
name: Grimaldi, Vincenzo
name: Trotta, Maria Consiglia
name: Sardu, Celestino
name: Sasso, Ferdinando Carlo
name: Scisciola, Lucia
name: Amarelli, Cristiano
name: Esposito, Salvatore
name: D’Amico, Michele
name: Golino, Paolo
name: De Feo, Marisa
name: Signoriello, Giuseppe
name: Paolisso, Pasquale
name: Gallinoro, Emanuele
name: Vanderheyden, Marc
name: Maiello, Ciro
name: Balestrieri, Maria Luisa
name: Barbato, Emanuele
name: Napoli, Claudio
name: Paolisso, Giuseppe
Publisher: name: figshare
Year: 2022
Subjects: subject: Biochemistry
subject: Medicine
subject: Cell Biology
subject: Molecular Biology
subject: Physiology
subject: FOS: Biological sciences
subject: Pharmacology
subject: 39999 Chemical Sciences not elsewhere classified
subject: FOS: Chemical sciences
subject: Cancer

description: Additional file 1: Figure S1. Western blot analysis of GlycACE2. Representative immunoblotting of recombinant hACE2 protein (ab151852, Abcam) after in vitro long-term exposure to glucose 120 mM was separated on SDS-PAGE by using 7% gels in reducing and non-reducing conditions and then transferred on nitrocellulose membrane. Membrane was incubated with specific primary antibody against GlycACE2 (1:1000) (#4355, Cell Signaling Technology). Molecular weight indicators are displayed at the center. Figure S2. Ejection fraction, TAPSE, and the E/e′ at week 1 (Basal) and week 48 (follow-up) in nondiabetic and diabetic patients treated with ACE-inhibitors (ACE-I) and angiotensin receptor blocker (ARB). Data are mean ± SD. *P &lt; 0.05 vs non-diabetics, §P &lt; 0.05 vs basal values. Figure S3. GlycACE2 at week 1 (Basal) and week 48 (Follow-up) in the diabetic patients with good glycemic control (HbA1c &lt; 7%) and diabetic patients with poor glycemic control (HbA1c ≥ 7%) treated with ACE-inhibitors (ACE-I) and angiotensin receptor blocker (ARB). Data are mean ± SD. *P &lt; 0.05 vs non-diabetics, §P &lt; 0.05 vs basal values. Figure S4. A Angiotensin-1–9 (Ang-1–9), Ang 1–7, Mas receptor (MasR), Nuclear factor of activated T-cells (NFAT), in explanted hearts (HTX) at week 1 (Basal) and week 48 (Follow-up) from HTX, in nondiabetic and diabetic patients, treated with ACE-inhibitors (ACE-I) and angiotensin receptor blocker (ARB). B Ang-1–9, Ang 1–7, MasR, and NFAT, in explanted hearts (HTX) at week 1 (Basal) and week 48 (Follow-up) from HTX,in the diabetic patients with good glycemic control (HbA1c &lt; 7%) and diabetic patients with poor glycemic control (HbA1c ≥ 7%) treated with ACE-inhibitors (ACE-I) and angiotensin receptor blocker (ARB). Data are mean ± SD. *P &lt; 0.05 vs non-diabetics, §P &lt; 0.05 vs basal values. Figure S5. Fibrosis percentage in explanted hearts (HTX), at week 1 (Basal) and week 48 (follow-up) from HTX, in the diabetic patients with good glycemic control (HbA1c &lt; 7%) and diabetic patients with poor glycemic control (HbA1c ≥ 7%) treated with ACE-inhibitors (ACE-I) and angiotensin receptor blocker (ARB). Data are mean ± SD. *P &lt; 0.05 vs non-diabetics, §P &lt; 0.05 vs basal values. Table S1. Multivariate linear regression analysis with GlycACE2 as dependent variable.