Evidence map›Paper›PMID 26681925›Full record

ArticleInternational journal of biological sciences2015

Krüppel-Like Factor 5 Promotes Epithelial Proliferation and DNA Damage Repair in the Intestine of Irradiated Mice.

Ming Li, Yuan Gu, Yan-Chao Ma, Zeng-Fu Shang, Chang Wang, Fen-Ju Liu, Jian-Ping Cao, Hua-Jing Wan, Xue-Guang Zhang

Abstract read
In one paragraph

Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Ming Li1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Yuan Gu1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Yan-Chao Ma3. Institute of Medical Biotechnology, Medical College of Soochow University, Suzhou, Jiangsu 215007, China ; 4. Jiangsu Stem Cell Key Laboratory, Medical College of Soochow University, Suzhou, Jiangsu 215007, China.
Zeng-Fu Shang1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Chang Wang1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Fen-Ju Liu1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Jian-Ping Cao1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu 215123, China ; 2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, China.
Hua-Jing Wan5. Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases and Birth Defects of the Ministry of Education, West China Institute of Women and Children's Health, and Department of Pediatrics, Huaxi Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Xue-Guang Zhang3. Institute of Medical Biotechnology, Medical College of Soochow University, Suzhou, Jiangsu 215007, China ; 4. Jiangsu Stem Cell Key Laboratory, Medical College of Soochow University, Suzhou, Jiangsu 215007, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsHigh doses of radiation induce severe DNA damage in intestinal epithelial cells, especially crypt cells, and cause intestinal injury, but the underlying molecular mechanisms remain unclear. Krüppel-like factor 5 (KLF5), a zinc finger-containing transcription factor, is induced by various stress stimuli and is involved in cell proliferation and survival. The role of KLF5 in radiation-induced intestinal injury was investigated here.

methodsWild type mice were treated with 8 or 15 Gy total body irradiation (TBI). KLF5 content and cellular localization in the small intestines of irradiated mice were detected by Western blot and immunohistochemical analysis. Mice with intestinal-specific knockdown of KLF5 (Vil-Cre; Klf5(fl/+) mice) were generated and their response to radiation was compared with controls. Morphological changes were determined by hematoxylin and eosin staining. Proliferation was examined by Ki67 immunostaining. The molecular response of the small intestine after KLF5 knockdown was investigated using microarrays.

resultsKLF5 expression correlated with the progression of intestinal damage. Decreased levels of KLF5 in the gut were associated with increased damage to the intestinal mucosa and reduced epithelial proliferation after TBI. Our microarray data disclosed that KLF5 knockdown down-regulated genes related to DNA damage repair pathways such as nucleotide excision repair, mismatch repair, non-homologous end joining and the Fanconi anemia pathway, which may suggest a novel function of KLF5.

conclusionsOur study illustrates that KLF5 may modulate DNA repair pathways to prevent intestinal injury induced by TBI. KLF5 signaling provides a novel field for identification of potential therapeutic targets for the treatment of radiation-induced intestinal damage.

Indexed as

DNA DamageDNA RepairAnimalsCell ProliferationDown-RegulationIntestinal MucosaIntestine, SmallKruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLKlf5 protein, mouseKruppel-Like Transcription Factorsintestinal injuryionizing radiationKrüppel-like factor 5mouse

Identifiers

PMID26681925
PMCPMC4672003

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.