PMID- 31929856
OWN - NLM
STAT- MEDLINE
DCOM- 20200619
LR  - 20231113
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2019
DP  - 2019
TI  - The Oxidative Stress-Induced miR-200c Is Upregulated in Psoriasis and Correlates 
      with Disease Severity and Determinants of Cardiovascular Risk.
PG  - 8061901
LID - 10.1155/2019/8061901 [doi]
LID - 8061901
AB  - Psoriasis is a chronic inflammatory skin disease associated with reactive oxygen 
      species (ROS) increase and a higher risk of cardiovascular (CV) events. We 
      previously showed that the miR-200 family (miR-200s) is induced by ROS, miR-200c 
      being the most upregulated member responsible for apoptosis, senescence, ROS 
      increase, and nitric oxide decrease, finally causing endothelial dysfunction. 
      Moreover, circulating miR-200c increases in familial hypercholesterolemic 
      children and in plaques and plasma of atherosclerotic patients, two pathologies 
      associated with increased ROS. Given miR-200s' role in endothelial dysfunction, 
      ROS, and inflammation, we hypothesized that miR-200s were modulated in lesional 
      skin (LS) and plasma of psoriatic patients (Pso) and that their levels correlated 
      with some CV risk determinants at a subclinical level. All Pso had severe 
      psoriasis, i.e., Psoriasis Area and Severity Index (PASI) > 10, and one of the 
      following: at least two systemic psoriasis treatments, age at onset < 40 years, 
      and disease duration > 10 years. RNA was extracted from plasma (Pso, N = 29; 
      Ctrl, N = 29) and from nonlesional skin (NLS) and LS of 6 Pso and 6 healthy 
      subject skin (HS) biopsies. miR-200 levels were assayed by quantitative RT-PCR. 
      We found that all miR-200s were increased in LS vs. NLS and miR-200c was the most 
      expressed and upregulated in LS vs. HS. In addition, circulating miR-200c and 
      miR-200a were upregulated in Pso vs. Ctrl. Further, miR-200c positively 
      correlated with PASI, disease duration, left ventricular (LV) mass, LV relative 
      wall thickness (RWT), and E/e', a marker of diastolic dysfunction. Multiple 
      regression analysis indicates a direct association between miR-200c and both RWT 
      and LV mass. Circulating miR-200a correlated positively only with LV mass and 
      arterial pressure augmentation index, a measure of stiffness, although the 
      correlations were nearly significant (P = 0.06). In conclusion, miR-200c is 
      upregulated in LS and plasma of Pso, suggesting its role in ROS increase and 
      inflammation associated with CV risk in psoriasis.
CI  - Copyright (c) 2019 A. Magenta et al.
FAU - Magenta, A
AU  - Magenta A
AUID- ORCID: 0000-0002-9054-337X
AD  - Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy.
FAU - D'Agostino, M
AU  - D'Agostino M
AD  - Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy.
FAU - Sileno, S
AU  - Sileno S
AUID- ORCID: 0000-0002-2036-2071
AD  - Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy.
FAU - Di Vito, L
AU  - Di Vito L
AD  - Unit of Cardiology, IDI-IRCCS, Rome, Italy.
FAU - Uras, C
AU  - Uras C
AD  - Unit of Cardiology, IDI-IRCCS, Rome, Italy.
FAU - Abeni, D
AU  - Abeni D
AD  - Clinical Epidemiology Unit, IDI-IRCCS, Rome, Italy.
FAU - Martino, F
AU  - Martino F
AD  - Department of Pediatrics, Sapienza University of Rome, Italy.
FAU - Barilla, F
AU  - Barilla F
AD  - Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and 
      Geriatric Sciences, Sapienza University of Rome, Italy.
FAU - Madonna, S
AU  - Madonna S
AD  - Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy.
FAU - Albanesi, C
AU  - Albanesi C
AUID- ORCID: 0000-0002-7537-6833
AD  - Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy.
FAU - Napolitano, M
AU  - Napolitano M
AD  - Clinical Epidemiology Unit, IDI-IRCCS, Rome, Italy.
FAU - Capogrossi, M C
AU  - Capogrossi MC
AD  - Division of Cardiology, Johns Hopkins University, Johns Hopkins Bayview Medical 
      Center, Baltimore, MD, USA.
AD  - Laboratory of Cardiovascular Science, National Institute on Aging (NIA), National 
      Institutes of Health (NIH), Baltimore, MD, USA.
FAU - Melillo, G
AU  - Melillo G
AD  - Unit of Cardiology, IDI-IRCCS, Rome, Italy.
LA  - eng
PT  - Journal Article
DEP - 20191219
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Biomarkers)
RN  - 0 (MIRN200 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Biomarkers
MH  - Cardiovascular Diseases/*epidemiology
MH  - Disease Progression
MH  - Endothelium, Vascular/*physiology
MH  - Female
MH  - Humans
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Middle Aged
MH  - Oxidative Stress
MH  - Psoriasis/epidemiology/*genetics
MH  - Reactive Oxygen Species/metabolism
MH  - Risk
MH  - Severity of Illness Index
MH  - Skin/*metabolism/pathology
MH  - Up-Regulation
PMC - PMC6939435
COIS- The authors declare no conflict of interest.
EDAT- 2020/01/14 06:00
MHDA- 2020/06/20 06:00
PMCR- 2019/12/19
CRDT- 2020/01/14 06:00
PHST- 2019/06/20 00:00 [received]
PHST- 2019/12/05 00:00 [accepted]
PHST- 2020/01/14 06:00 [entrez]
PHST- 2020/01/14 06:00 [pubmed]
PHST- 2020/06/20 06:00 [medline]
PHST- 2019/12/19 00:00 [pmc-release]
AID - 10.1155/2019/8061901 [doi]
PST - epublish
SO  - Oxid Med Cell Longev. 2019 Dec 19;2019:8061901. doi: 10.1155/2019/8061901. 
      eCollection 2019.