scholarly journals Niacin mitigates rumen epithelial damage in vivo by inhibiting rumen epithelial cell apoptosis on a high concentrate diet

2021 ◽  
Author(s):  
Zhen Gao ◽  
Yanjiao Li ◽  
Chao Xu ◽  
Dan Luo ◽  
Qinghua Qiu ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Antioxidant Capacity ◽  
Inflammatory Cytokines ◽  
Cell Apoptosis ◽  
Volatile Fatty Acids ◽  
Epithelial Damage ◽  
Rumen Epithelium ◽  
Rumen Ph ◽  
Epithelial Cell Apoptosis

Abstract To investigate the effects of niacin on rumen fermentation, rumen epithelial antioxidant activity, and rumen epithelial cell apoptosis on high concentrate (HC) diets, nine male Hu sheep were randomly divided into: low concentrate diet (LC; concentrate : forage (C:F) = 20:80, high concentrate diet (HC; C:F = 80:20), and HCN diet (HC diet + niacin at 800 mg/kg diet air-dry matter). Compared with the LC group, the HC group had a lower rumen pH, increased volatile fatty acids and lactic acid in the rumen, reduced activity of antioxidant enzymes and total antioxidant capacity, and increased malondialdehyde content in the rumen epithelium (P < 0.05). Rumen epithelial papilla morphology was decreased, and apoptosis-related indicators and serum inflammatory cytokines were increased in the HC group over the LC group (P < 0.05). Compared with the HC diet, the HCN diet increased rumen pH, rumen epithelium antioxidant capacity, and rumen epithelial papilla morphology, decreased rumen lactate content, serum inflammatory cytokines, and apoptosis-related indicators (P < 0.05). Therefore, adding 800 mg/kg niacin helped protect against rumen epithelial damage by avoiding drastic changes in the rumen environment and improved rumen epithelial antioxidant capacity to inhibit rumen epithelial cell apoptosis in sheep on a HC diet.

scholarly journals Effects of a progestogen on normal human breast epithelial cell apoptosis in vitro and in vivo

The Breast ◽  
2003 ◽  
Vol 12 (2) ◽  
pp. 142-149 ◽  
Author(s):  
J Desreux ◽  
F Kebers ◽  
A Noël ◽  
D Francart ◽  
H Van Cauwenberge ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Breast Epithelial Cell ◽  
Human Breast ◽  
Human Breast Epithelial Cell ◽  
Normal Human Breast ◽  
Epithelial Cell Apoptosis ◽  
Normal Human

IL-10 modulates intestinal damage and epithelial cell apoptosis in T cell-mediated enteropathy

2004 ◽  
Vol 287 (3) ◽  
pp. G599-G604 ◽  
Author(s):  
Pengfei Zhou ◽  
Cathy Streutker ◽  
Rajka Borojevic ◽  
Yufa Wang ◽  
Ken Croitoru
Keyword(s):  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Intestinal Tissue ◽  
Epithelial Cell Apoptosis

In vivo T cell activation by anti-CD3 monoclonal antibody (mAb) results in intestinal damage characterized by loss of villi and epithelial cell apoptosis. The role of the increased interleukin (IL)-10 released during this process is not clear. We assessed the effects of IL-10 on T cell-induced mucosal damage in vivo using IL-10-deficient C57BL/6 [IL-10 knockout (KO)] mice. IL-10 KO and wild-type C57BL/6 mice were injected with anti-CD3 mAb and observed for diarrhea. Changes in serum cytokine levels were measured by ELISA. Histological changes and epithelial cell apoptosis were analyzed on hematoxylin- and eosin-stained tissue sections. Fas expression on intestinal epithelial cells was assessed by flow cytometry analysis of freshly isolated intestinal epithelial cells. Anti-CD3-treated IL-10 KO mice developed more severe diarrhea, a greater loss of intestinal villi, and an increase in the numbers of apoptotic cells in the crypt epithelium. This difference in IL-10 KO mice was associated with an increase in serum tumor necrosis factor-α and interferon-γ levels and with an increase in Fas expression on fresh, isolated, small intestinal epithelial cells. In addition, the enhanced intestinal tissue damage induced by anti-CD3 in IL-10 KO mice was significantly diminished by treatment with recombinant murine IL-10. Therefore, the lack of IL-10 allowed for an increased T cell-induced intestinal tissue damage, and this was associated with an increase in T cell cytokine release and an increase in epithelial cell Fas expression.

scholarly journals Loss of miR-24-3p promotes epithelial cell apoptosis and impairs the recovery from intestinal inflammation

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Artin Soroosh ◽  
Kai Fang ◽  
Jill M. Hoffman ◽  
Ivy K. M. Law ◽  
Elizabeth Videlock ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Intestinal Inflammation ◽  
Loss Of Function ◽  
Epithelial Cell Apoptosis ◽  
Vitro Analysis ◽  
Double Blinded ◽  
Active Inflammation

AbstractWhile apoptosis plays a significant role in intestinal homeostasis, it can also be pathogenic if overactive during recovery from inflammation. We recently reported that microRNA-24-3p (miR-24-3p) is elevated in the colonic epithelium of ulcerative colitis patients during active inflammation, and that it reduced apoptosis in vitro. However, its function during intestinal restitution following inflammation had not been examined. In this study, we tested the influence of miR-24-3p on mucosal repair by studying recovery from colitis in both novel miR-24-3p knockout and miR-24-3p-inhibited mice. We observed that knockout mice and mice treated with a miR-24-3p inhibitor had significantly worsened recovery based on weight loss, colon length, and double-blinded histological scoring. In vivo and in vitro analysis of miR-24-3p inhibition in colonic epithelial cells revealed that inhibition promotes apoptosis and increases levels of the pro-apoptotic protein BIM. Further experiments determined that silencing of BIM reversed the pro-apoptotic effects of miR-24-3p inhibition. Taken together, these data suggest that miR-24-3p restrains intestinal epithelial cell apoptosis by targeting BIM, and its loss of function is detrimental to epithelial restitution following intestinal inflammation.

scholarly journals Mammalian STE20-Like Kinase 1 Deletion Alleviates Renal Ischaemia-Reperfusion Injury via Modulating Mitophagy and the AMPK-YAP Signalling Pathway

2018 ◽  
Vol 51 (5) ◽  
pp. 2359-2376 ◽  
Author(s):  
Junxia Feng ◽  
Hongyan Li ◽  
Yunfang Zhang ◽  
Qi Wang ◽  
Shili Zhao ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Tubular Epithelial Cell ◽  
Signalling Pathway ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Epithelial Cell Apoptosis

Background/Aims: The aim of our study is to investigate the molecular mechanism by which mammalian STE20-like kinase 1 (Mst1) participates in renal I/R injury through modifying mitophagy and the AMPK-YAP signalling pathway. Methods: WT mice and Mst1-knockout mice were subjected to renal ischaemia-reperfusion (I/R) in vivo. In vitro, the hypoxia-reoxygenation model was used with renal tubular epithelial cells to mimic renal I/R injury. Mitochondrial function was monitored via western blotting and immunofluorescence. Pathway blocker and siRNA knockout technology were used to establish the role of the AMPK-YAP signalling pathway in Mst1-mediated mitochondrial apoptosis in the setting of renal I/R injury. Results: Our data demonstrated that Mst1 expression was upregulated in response to renal I/R injury in vivo, and a higher Mst1 content was positively associated with renal dysfunction and more tubular epithelial cell apoptosis. However, genetic ablation of Mst1 improved renal function, alleviated reperfusion-mediated tubular epithelial cell apoptosis, and attenuated the vulnerability of kidney to I/R injury. In vitro, Mst1 upregulation induced mitochondrial damage including mitochondrial potential reduction, ROS overloading, cyt-c liberation and caspase-9 apoptotic pathway activation. At the molecular levels, I/R-mediated mitochondrial damage via repressing mitophagy and Mst1 suppressed mitophagy via inactivating AMPK signalling pathway and dowregulating OPA1 expression. Re-activation of AMPK-YAP-OPA1 signalling pathway provided a survival advantage for the tubular epithelial cell in the context of renal I/R injury by repressing mitochondrial fission. Conclusion: Overall, our results demonstrate that the pathogenesis of renal I/R injury is closely associated with an increase in Mst1 expression and the inactive AMPK-YAP-OPA1 signalling pathway. Based on this, strategies to repress Mst1 expression and activate mitophagy could serve as therapeutic targets to treat kidney ischaemia-reperfusion injury.

scholarly journals Fas (CD95) Induces Alveolar Epithelial Cell Apoptosis in Vivo

2001 ◽  
Vol 158 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Gustavo Matute-Bello ◽  
Robert K. Winn ◽  
Mechthild Jonas ◽  
Emil Y. Chi ◽  
Thomas R. Martin ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial ◽  
Epithelial Cell Apoptosis
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