2017
DOI: 10.1111/jgh.13461
|View full text |Cite
|
Sign up to set email alerts
|

A phenotype of IGFBP‐3 knockout mice revealed by dextran sulfate‐induced colitis

Abstract: Our data demonstrate that IGFBP-3 influences severity of DSS-induced colitis. The observations suggest that in the absence of IGFBP-3, enhanced IGF bioactivity leads to increased epithelial proliferation and mucosal barrier repair, thereby lessening inflammation.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
5
0

Year Published

2017
2017
2023
2023

Publication Types

Select...
5
1

Relationship

0
6

Authors

Journals

citations
Cited by 7 publications
(6 citation statements)
references
References 25 publications
1
5
0
Order By: Relevance
“…IGFBP -3 knockout mice demonstrated a less active inflammatory state and lower levels of IL -6, TNF -α, and IL -1β, as well as increased proliferation of intestinal endothelial cells leading to repair of the endothelial barrier, which might confirm the role of the IGF axis in the development of the inflammatory state in patients with IBD. 30 In turn, an experimental study performed by Harris et al 31 in mice with colitis induced by dextran sodium sulfate showed a decrease in the level of plasma IGF -1; these results are concordant with our observations in adult patients with IBD. In conclusion, our results show that the IGF system is disrupted in patients with IBD.…”
Section: Patientssupporting
confidence: 81%
“…IGFBP -3 knockout mice demonstrated a less active inflammatory state and lower levels of IL -6, TNF -α, and IL -1β, as well as increased proliferation of intestinal endothelial cells leading to repair of the endothelial barrier, which might confirm the role of the IGF axis in the development of the inflammatory state in patients with IBD. 30 In turn, an experimental study performed by Harris et al 31 in mice with colitis induced by dextran sodium sulfate showed a decrease in the level of plasma IGF -1; these results are concordant with our observations in adult patients with IBD. In conclusion, our results show that the IGF system is disrupted in patients with IBD.…”
Section: Patientssupporting
confidence: 81%
“…On the contrary, metformin administration was effective in reducing number of tumors, the composition of resident inflammatory cells and other inflammatory scores, and the incidence of adenocarcinomas in the colon of AOM + DSS treated mice after 16-weeks. Similarly, the chemopreventive effect of metformin has been previously demonstrated [22] and the effects of IGFBP3 knockout and metformin were observed in a murine model of ulcerative colitis, showing significantly reduced colitis [30].…”
Section: Discussionmentioning
confidence: 78%
“…LYC was extracted from softgels and homogenized with NaCl 0.9% to provide the corresponding concentration; groups 6–7 (LYC 20 and LYC 50, n = 7) received 20 and 50 mg kg −1 of LYC, respectively. Metformin (1, 1-dimethylbiguanide hydrochloride) has been reported to provide in vivo and in vitro anti-inflammatory effects through inhibition of NF-κB signaling [22,30,44]; thus, a positive control group was included, and animals in group 8 (Metformin, n = 7) received 600 mg·kg −1 of metformin (Merck company, Naucalpan de Juárez, Edo de México, MEX), dissolved in NaCl 0.9%. The corresponding treatments were prepared daily and gavaged every morning (0.2 mL total volume) to all mice throughout the 16 weeks, with the exceptions of weeks 5 and 6.…”
Section: Methodsmentioning
confidence: 99%
“…IGFBP-3 is a growth factor downregulating angiogenesis [ 52 ]. In addition, upregulation of IGFBP-3 is correlated with the improvement of colitic mice, and IGFBP-3 knockout animals are resistant to DSS-induced inflammation of the colon [ 53 , 54 ]. Interestingly, the level of IGFBP-3 in the intestine did not change under the influence of H. polygyrus in healthy mice.…”
Section: Discussionmentioning
confidence: 99%