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Tytuł pozycji:

Inhibition of microRNA-150-5p alleviates cardiac inflammation and fibrosis via targeting Smad7 in high glucose-treated cardiac fibroblasts.

Tytuł:
Inhibition of microRNA-150-5p alleviates cardiac inflammation and fibrosis via targeting Smad7 in high glucose-treated cardiac fibroblasts.
Autorzy:
Che H; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.; Translational Medicine Research and Cooperation Center of Northern China, Heilongjiang Academy of Medical Sciences, Harbin, Heilongjiang, China.
Wang Y; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Li Y; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Lv J; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Li H; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Liu Y; Department of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, China.
Dong R; Department of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, China.
Sun Y; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Xu X; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Zhao J; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Wang L; Department of Endocrinology, The Second affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Źródło:
Journal of cellular physiology [J Cell Physiol] 2020 Nov; Vol. 235 (11), pp. 7769-7779. Date of Electronic Publication: 2019 Nov 11.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: New York, NY : Wiley-Liss
Original Publication: Philadelphia, Wistar Institute of Anatomy and Biology.
MeSH Terms:
Diabetic Cardiomyopathies/*metabolism
Fibroblasts/*pathology
Glucose/*toxicity
MicroRNAs/*metabolism
Smad7 Protein/*metabolism
Animals ; Cells, Cultured ; Diabetic Cardiomyopathies/pathology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibrosis ; Gene Expression Regulation ; Hyperglycemia/metabolism ; Hyperglycemia/pathology ; Inflammation/chemically induced ; Inflammation/metabolism ; Inflammation/pathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Signal Transduction/physiology
References:
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Contributed Indexing:
Keywords: TGF-β1/Smad; diabetic cardiomyopath; fibrosis; inflammation; microRNA-150-5p
Substance Nomenclature:
0 (MIRN150 microRNA, rat)
0 (MicroRNAs)
0 (Smad7 Protein)
0 (Smad7 protein, rat)
IY9XDZ35W2 (Glucose)
Entry Date(s):
Date Created: 20191112 Date Completed: 20210308 Latest Revision: 20210308
Update Code:
20240105
DOI:
10.1002/jcp.29386
PMID:
31710102
Czasopismo naukowe
Hyperglycemia-induced cardiac fibrosis is a prominent characteristic of diabetic cardiomyopathy. Changes in proinflammatory cytokines have been shown to lead to cardiac fibrosis in patients with diabetes mellitus. This study aimed to investigate the role of miR-150-5p in mediating cardiac inflammation and fibrosis in cardiac fibroblasts (CFs). Herein, we found that high-glucose (HG) treatment significantly induced cardiac inflammation, as manifested by increased proinflammatory cytokine production (IL-1β) and NF-κB activity in CFs. Moreover, HG markedly aggravated cardiac fibrosis and increased levels of fibrotic markers (CTGF, FN, α-SMA) and extracellular matrix proteins (Col-I, Col-III) in CFs. At the same time, HG disturbed the TGF-β1/Smad signaling pathway, as evidenced by increases in TGF-β1 and p-Smad2/3 levels and decreases in Smad7 levels in CFs. Furthermore, we found that miR-150-5p was upregulated by HG, which negatively regulated Smad7 expression at the posttranscription level. Further study demonstrated that cardiac inflammation and fibrosis in CFs were corrected following miR-150-5p knockdown, but exacerbated by miR-150-5p overexpression. These data indicated that miR-150-5p inhibition could ameliorate NF-κB-related inflammation and TGF-β1/Smad-induced cardiac fibrosis through targeting Smad7. Thus, miR-150-5p may be a novel promising target for treating diabetic cardiomyopathy.
(© 2019 Wiley Periodicals, Inc.)

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