ArticleMolecular medicine reports2018
FKBP11 protects intestinal epithelial cells against inflammation‑induced apoptosis via the JNK‑caspase pathway in Crohn's disease.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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15 citing papers in PubMed, 19 citations in OpenAlex.
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- Lactoferrin Alleviated AFM1-Induced Apoptosis in Intestinal NCM 460 Cells through the Autophagy Pathway.Foods (Basel, Switzerland) · 2021Article
- Apple Polyphenols Extract (APE) Alleviated Dextran Sulfate Sodium Induced Acute Ulcerative Colitis and Accompanying Neuroinflammation via Inhibition of Apoptosis and Pyroptosis.Foods (Basel, Switzerland) · 2021Article
- Inositol-Requiring Kinase 1 Regulates Apoptosis via Inducing Endoplasmic Reticulum Stress in Colitis Epithelial Cells.Digestive diseases and sciences · 2021Article
- Identification and Development of a Novel 4-Gene Immune-Related Signature to Predict Osteosarcoma Prognosis.Frontiers in molecular biosciences · 2020Article
- Effect of Berberine fromEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Chlorogenic Acid Attenuates Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice through MAPK/ERK/JNK Pathway.BioMed research international · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum (ER) stress in intestinal epithelial cells (IECs) has an important role in the pathogenesis of Crohn's disease (CD). FK506 binding protein 11 (FKBP11), a member of the peptidyl‑prolyl cis‑trans isomerase family, is involved in the unfolded protein response (UPR) and is closely associated with inflammation. Previous bioinformatics analysis revealed a potential association between FKBP11 and human CD. Thus, the present study aimed to investigate the potential significance of FKBP11 in IEC homeostasis and CD. In the present study, increased expression of FKBP11 was detected in the intestinal inflammatory tissues of patients with CD. Furthermore, the results of the present study revealed that overexpression of FKBP11 was accompanied by increased expression levels of the ER stress marker 78 kDa glucose‑regulated protein in the colon tissues of a 2, 4, 6‑trinitrobenzenesulphonic acid‑induced mouse colitis model. Using interferon‑γ (IFN‑γ)/tumor necrosis factor‑α (TNF‑α)‑stimulated IECs as an ER stress and apoptosis cell model, the associated of FKBP11 with ER stress and apoptosis levels was confirmed in IECs. Overexpression of FKBP11 was revealed to significantly attenuate the elevated expression of pro‑apoptotic proteins (Bcl2 associated X apoptosis regulator, caspase‑12 and active caspase‑3), suppress the phosphorylation of c‑Jun N‑terminal kinase (JNK), and decrease apoptosis of IFN‑γ/TNF‑α stimulated IECs. Knockdown of FKBP11 by transfection with small interfering RNA further validated the aforementioned results. In conclusion, these results suggest that the UPR protein FKBP11 may protect IECs against IFN‑γ/TNF‑α induced apoptosis by inhibiting the ER stress‑associated JNK/caspase apoptotic pathway in CD.
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