2020
DOI: 10.1016/j.jss.2020.03.037
|View full text |Cite
|
Sign up to set email alerts
|

Inhibition of miR-16 Ameliorates Inflammatory Bowel Disease by Modulating Bcl-2 in Mouse Models

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
6
0

Year Published

2021
2021
2022
2022

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 6 publications
(6 citation statements)
references
References 34 publications
0
6
0
Order By: Relevance
“…(2011) and Chen et al. (2020) revealed similar results that miR-150 or miR-16 can downregulate the expression of Bcl-2 to disrupt colonic epithelium in DSS-induced mouse IBD models ( 69 , 70 ). TGF-β may downregulate miR-29b expression, which will inhibit the gene expression of IL-6/Mcl-1 (an anti-fibrotic mediator) or the IL-8 / Mcl-1 axis, and then lead to increased collagen deposition and promote intestinal fibrosis in patients with CD ( 71 ).…”
Section: Mirnas and Pathogenesis-related Signaling Pathways In Ibdmentioning
confidence: 78%
See 1 more Smart Citation
“…(2011) and Chen et al. (2020) revealed similar results that miR-150 or miR-16 can downregulate the expression of Bcl-2 to disrupt colonic epithelium in DSS-induced mouse IBD models ( 69 , 70 ). TGF-β may downregulate miR-29b expression, which will inhibit the gene expression of IL-6/Mcl-1 (an anti-fibrotic mediator) or the IL-8 / Mcl-1 axis, and then lead to increased collagen deposition and promote intestinal fibrosis in patients with CD ( 71 ).…”
Section: Mirnas and Pathogenesis-related Signaling Pathways In Ibdmentioning
confidence: 78%
“…Chen et al. (2020) indicated that the IP administration of miR-16 antagomir upregulated the Bcl-2 expression and ameliorates intestine function in 3% DSS-induced mice ( 69 ). In contrast, Zhang et al.…”
Section: Mirna-related Potential Therapies To Ibdmentioning
confidence: 99%
“…In this case, miRNAs complementary antisense oligonucleotides or miRNA mimics can be potential therapeutics that abolish or mimic miRNA’s function and, therefore, block inflammatory progression, modulate cytokines or chemokine hemostasis and increase the treatment sensitivity of conventional therapies. As such, miRNAs are used for modulating hypoxia ( 183 , 184 ) and the inflammatory response by targeting major inflammatory pathways ( 185 189 ) and essential molecules, including tight junction proteins that maintain the integrity of the membrane ( 74 , 190 , 191 ).…”
Section: Discussionmentioning
confidence: 99%
“…Consistently, the overexpression of miR-135a in colonic epithelial cells prevented apoptosis and inflammation by inhibiting the expression of apoptotic factor Bax and enhancing the expression of anti-apoptotic factor Bcl-2 via HIF-1α [ 131 ]. Another study found a negative correlation between miR-16 and Bcl-2 expression in Caco-2 cells and in the colonic mucosa of DSS-treated mice [ 107 ]. Further investigation in 3% DSS induced colitis mice (two weeks) with the intraperitoneal administration of anti-miR-16 (dose: 5 mg/kg, twice per week) alleviated colitis and reduced proinflammatory cytokines in comparison to PBS-treated DSS controls [ 107 ].…”
Section: Microrna As a Therapeutic Target In Ibdmentioning
confidence: 99%
“…Another study found a negative correlation between miR-16 and Bcl-2 expression in Caco-2 cells and in the colonic mucosa of DSS-treated mice [ 107 ]. Further investigation in 3% DSS induced colitis mice (two weeks) with the intraperitoneal administration of anti-miR-16 (dose: 5 mg/kg, twice per week) alleviated colitis and reduced proinflammatory cytokines in comparison to PBS-treated DSS controls [ 107 ].…”
Section: Microrna As a Therapeutic Target In Ibdmentioning
confidence: 99%