In:
PLOS Neglected Tropical Diseases, Public Library of Science (PLoS), Vol. 17, No. 7 ( 2023-7-25), p. e0011520-
Abstract:
Liver fibrosis is one of the histopathological characters during Echinococcus multilocularis infection. The activation of hepatic stellate cells (HSCs) is a key event in the development of liver fibrosis. However, the molecular mechanism of HSC activation in the E . multilocularis infection-induced liver fibrosis remains largely unclear. Here, we reported that mmu-miR-342-3p was most dominantly expressed in HSCs and was upregulated in the HSCs in response to E . multilocularis infection. We further showed that mmu-miR-342-3p was able to bind to the 3’ UTR of the Zbtb7a gene and regulated its expression. Moreover, mmu-miR-342-3p expression was negatively correlated with its target gene Zbtb7a in HSCs during E . multilocularis infection. Knockdown of mmu-miR-342-3p promoted the expression of Gfap in the activated HSCs in vitro . In the E . multilocularis -infected mice, knockdown of mmu-miR-342-3p suppressed the expression of α-Sma , Col1α1 , and TGF-β but promoted the expression of Gfap . Therefore, mmu-miR-342-3p is a key regulator for activation of HSCs, and inhibiting mmu-miR-342-3p to suppressed Zbtb7a-mediated TGF-β signaling in activated HSCs could be a novel strategy to treat liver fibrosis induced by E . multilocularis .
Type of Medium:
Online Resource
ISSN:
1935-2735
DOI:
10.1371/journal.pntd.0011520
DOI:
10.1371/journal.pntd.0011520.g001
DOI:
10.1371/journal.pntd.0011520.g002
DOI:
10.1371/journal.pntd.0011520.g003
DOI:
10.1371/journal.pntd.0011520.g004
DOI:
10.1371/journal.pntd.0011520.g005
DOI:
10.1371/journal.pntd.0011520.g006
DOI:
10.1371/journal.pntd.0011520.s001
DOI:
10.1371/journal.pntd.0011520.s002
DOI:
10.1371/journal.pntd.0011520.s003
DOI:
10.1371/journal.pntd.0011520.s004
DOI:
10.1371/journal.pntd.0011520.s005
DOI:
10.1371/journal.pntd.0011520.s006
DOI:
10.1371/journal.pntd.0011520.s007
DOI:
10.1371/journal.pntd.0011520.s008
DOI:
10.1371/journal.pntd.0011520.s009
DOI:
10.1371/journal.pntd.0011520.r001
DOI:
10.1371/journal.pntd.0011520.r002
DOI:
10.1371/journal.pntd.0011520.r003
DOI:
10.1371/journal.pntd.0011520.r004
DOI:
10.1371/journal.pntd.0011520.r005
DOI:
10.1371/journal.pntd.0011520.r006
DOI:
10.1371/journal.pntd.0011520.r007
DOI:
10.1371/journal.pntd.0011520.r008
DOI:
10.1371/journal.pntd.0011520.r009
DOI:
10.1371/journal.pntd.0011520.r010
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2429704-5
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