Additional file 2: of Inhibition of the RhoGTPase Cdc42 by ML141 enhances hepatocyte differentiation from human adipose-derived mesenchymal stem cells via the Wnt5a/PI3K/miR-122 pathway: impact of the age of the donor

Table S2. Characteristics of the studied population (results are expressed as the mean ± SEM). (DOCX 21 kb

Additional file 1: of Inhibition of the RhoGTPase Cdc42 by ML141 enhances hepatocyte differentiation from human adipose-derived mesenchymal stem cells via the Wnt5a/PI3K/miR-122 pathway: impact of the age of the donor

Table S1. Primer sequences used for quantitative RT-PCR. (DOCX 19 kb

Characteristics of the study population in the healthy group ⁽¹⁾ (results are expressed as the mean ± SEM).

<p>⁽¹⁾ HH group for hypertension and hypercholesterolemics subjects is considered with CAD historical and total cholesterol is > 250 mg/dL proportioned to elevated level of LDL and low HDL, and systolic /diastolic blood pressure is > 140/90 mm Hg.</p><p>⁽²⁾ Physically active: walking or doing other kinds of exercise at least once per week or self-report of moderate/intense level of activity in daily life. LDL: low density lipoprotein; HDL: high density lipoprotein; CAD: coronary artery disease.</p><p>Characteristics of the study population in the healthy group ⁽<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0127266#t001fn001" target="_blank">¹</a>⁾ (results are expressed as the mean ± SEM).</p

Profile of cytokines secretion in cases co-expressing or not ACE/PAI-1(Del/4G).

<p>Cytokines secretion in culture supernatants from peripheral blood mononuclear cells (PBMCs) obtained from the 6 healthy subjects not expressing the combined double risky alleles “Del” of ACE and “4G” of PAI-1 genes [Healthy-ACE/PAI-1(Del/4G)(-/-)], from 6 healthy subjects co-expressing Del/4G [Healthy-ACE/PAI-1(Del/4G)(+/+)] and from 6 patients HH co-expressing Del/4G [HH-ACE/PAI-1(Del/4G)(+/+)]. TNF-α (A), IFN-γ (B), IL-4 (C) and IL-10 (D) production were determined in triplicates (n = 24 for each group) and results are Mean ± SEM. *<i>P<0</i>.<i>05</i> and **<i>P<0</i>.<i>01</i>; Del/4G(+/+) <i>versus</i> Del/4G(-/-).</p

Distribution of atherosclerosis and venous thrombosis-related genes in the healthy group (n = 171) between populations co-expressing allele “Del” of ACE and “4G” of PAI-1(Del/4G,+/+): Allele’s frequencies.

<p><i>A</i>, Relative distribution of atherosclerosis related polymorphisms. <i>B</i>, Relative distribution of venous thrombosis related genes. Results are expressed as percentages ± SEM of the number of patients detected with or without mutation from the number of the studied population. Co-expression Del/4G(+/+) (detected in 113 patients) or absence of Del/4G(-/-) (only 6 patients not expressing alleles Del/4G) (Total population, n = 171).</p

Evaluation of the number of risk factor to occur by patient between the Healthy and the HH groups.

<p>Results are expressed as percentages of expressed gene’s mutation per (n) risk factor: 8(<i>A</i>), 7(<i>B</i>), 6(<i>C</i>), 5(<i>D</i>), 4(<i>E</i>) and 3(<i>F</i>). 12 polymorphisms are studied: Prothrombin FII(G20210A); FV-L(Leiden); FV-R2(R2); FXIII(V34L); MTHFR(C677T); MTHFR(A1298C); PAI-1(4G); ACE(Del); beta-fibrinogen FGB(-455G>A); HPA-1(b); ApoB(R3500Q); ApoE(E4).</p

Evaluation of the number of risk factors to occur by subject.

<p>(1) One risk factor is defined as a detected mutation per gene expression</p><p>Evaluation of the number of risk factors to occur by subject.</p

Kinetic evaluation of the levels of ACE and PAI-1 in the patient’s serum (results are expressed as the mean ± SEM).

<p>*<i>P<0</i>.<i>05</i>; I/D <i>versus</i> I/I.</p><p>^#<i>P<0</i>.<i>05</i>; D/D <i>versus</i> I/I.</p><p>^{# #}<i>P<0</i>.<i>01</i>; D/D <i>versus</i> I/I.</p><p>^&<i>P<0</i>.<i>05</i>; 4G/5G <i>versus</i> 5G/5G.</p><p>All comparisons were performed within the same group of healthy or HH.</p><p>Kinetic evaluation of the levels of ACE and PAI-1 in the patient’s serum (results are expressed as the mean ± SEM).</p

Effects of ramipril (RAMP) and atorvastatin (ATV) on cytokines, ACE and PAI-1 secretion.

<p>Culture supernatants from peripheral blood mononuclear cells (PBMCs) were obtained from the 6 healthy subjects not expressing the combined double risky alleles “Del” of ACE and “4G” of PAI-1 genes [Healthy-ACE/PAI-1(Del/4G)(-/-)], from 6 healthy subjects co-expressing Del/4G [Healthy-ACE/PAI-1(Del/4G)(+/+)] and from 6 patients HH co-expressing Del/4G [HH-ACE/PAI-1(Del/4G)(+/+)]. Cells were treated 48h with 10μM of RAMP and/or ATV. TNF-α (A), IFN-γ (B), IL-4 (C), IL-10 (D), ACE (E), PAI-1 (F) production were determined in triplicates (n = 24 for each group) and results are Mean ± SEM. ^§<i>P<0</i>.<i>05</i>; Del/4G(+/+) <i>versus</i> Del/4G(-/-).*<i>P<0</i>.<i>05</i> and **<i>P<0</i>.<i>01</i>; RAMP+ATV <i>versus</i> Control.</p

Distribution of risk factors that occur by gene’s mutations.

<p>Co-expression of mutations by patient detected in total population of the healthy group (n = 171) or the hypertensive hypercholesterolemic group (n = 144). Results are expressed as percentages of from the total number of the studied population.</p