0000000000311641
AUTHOR
Noemi Panzera
showing 6 related works from this author
Mesenchymal stem cells of Systemic Sclerosis patients, derived from different sources, show a profibrotic microRNA profiling
2019
AbstractSystemic Sclerosis (SSc) is a disease with limited therapeutic possibilities. Mesenchymal stem cells (MSCs)-therapy could be a promising therapeutic option, however the ideal MSCs source has not yet been found. To address this problem, we perform comparison between bone marrow (BM)-MSCs and adipose (A)-MSCs, by the miRs expression profile, to identify the gene modulation in these two MSCs source. MicroRNAs (miRs) are RNAs sequences, regulating gene expression and MSCs, derived from different tissues, may differently respond to the SSc microenvironment. The miRs array was used for the miRs profiling and by DIANA-mirPath tool we identified the biological functions of the dysregulated …
Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension
2020
Abstract Background Pulmonary arterial hypertension (PAH) is a severe complication of systemic sclerosis (SSc), associated with a progressive elevation in pulmonary vascular resistance and subsequent right heart failure and death. Due to unspecific symptoms, the diagnosis of PAH is often delayed. On this basis, it is of great value to improve current diagnostic methods and develop new strategies for evaluating patients with suspected PAH. Interleukin-32 (IL-32) is a proinflammatory cytokine expressed in damaged vascular cells, and the present study aimed to assess if this cytokine could be a new biomarker of PAH during SSc. Methods The IL-32 expression was evaluated in the sera and skin sam…
Blocking Jak/STAT signalling using tofacitinib inhibits angiogenesis in experimental arthritis
2021
Abstract Objective During rheumatoid arthritis (RA), the angiogenic processes, occurring with pannus-formation, may be a therapeutic target. JAK/STAT-pathway may play a role and the aim of this work was to investigate the inhibiting role of a JAK-inhibitor, tofacitinib, on the angiogenic mechanisms occurring during RA. Methods After ethical approval, JAK-1, JAK-3, STAT-1, STAT-3 and VEGF expression was evaluated on RA-synovial-tissues. In vitro, endothelial cells (ECs), stimulated with 20 ng/ml of VEGF and/or 1 μM of tofacitinib, were assessed for tube formation, migration and proliferation, by Matrigel, Boyden chamber assay and ki67 gene-expression. In vivo, 32 mice received collagen (coll…
Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibrobla…
2018
Abstract Background Fibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process. Methods After ethical approval was obtained, skin biopsies were co…
Additional file 2 of Blocking Jak/STAT signalling using tofacitinib inhibits angiogenesis in experimental arthritis
2021
Additional file 2: Supplementary material 2. Arthritis score evaluation. The histogram showed the median and the range of the arthritis score evaluated the day 35. The collagen induced a significant increase of arthritis score when compared to control group, and 30 mg/Kg/day of tofacitinib prevented the increase of arthritis score (**=p=0.001; ***= p
Additional file 1 of Blocking Jak/STAT signalling using tofacitinib inhibits angiogenesis in experimental arthritis
2021
Additional file 1: Supplementary material 1. Mice treatments. The first day (day 0) of the procedure, 64 DBA/1 J mice were divided in 2 groups. One control group (n=32) receiving saline solution and one CIA group (n=32) receiving 100 μg of bovine type II collagen, emulsified with an equal volume of Freund’s complete adjuvant. After 18 days, the control group received saline solution and CIA mice received type II collagen and Freund’s incomplete adjuvant. At the day 19, controls and CIA mice were divided into 2 subgroups: one receiving vehicle (n=16) and one receiving 30 mg/kg/day of tofacitinib (n=16). After 35 days the first collagen administration, the mice were sacrificed and the blood c…