Evidence map›Paper›PMID 25332219›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2015

Endoplasmic reticulum stress-mediated apoptotic pathway is involved in corpus luteum regression in rats.

Yanzhou Yang, Miao Sun, Yuanyuan Shan, Xiaomin Zheng, Huiming Ma, Wenzhi Ma, Zhisheng Wang, Xiuying Pei, Yanrong Wang

Open access · bronzeAbstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
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

22 citing papers in PubMed, 46 citations in OpenAlex.

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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 at 1 institution in 1 country.

Yanzhou YangDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Miao SunDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Yuanyuan ShanDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Xiaomin ZhengDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Huiming MaDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Wenzhi MaDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Zhisheng WangDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China.
Xiuying PeiDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China nxykdyang@163.com 4083304@163.com peixuiying@163.com.
Yanrong WangDepartment of Histology and Embryology, Ningxia Medical University, Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Key Laboratory of Reproduction and Genetics in Ningxia, Yinchuan, P.R. China nxykdyang@163.com 4083304@163.com peixuiying@163.com.
Ningxia University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS), which is a novel pathway of regulating cellular apoptosis and the function of ERS during corpus luteum (CL) regression, is explored. Early-luteal stage (day 2), mid-luteal stage (day 7), and late-luteal stage (day 14 and 20) were induced, and the apoptosis of luteal cells was detected by a terminal 2'-deoxyuridine 5'-triphosphate nick-end labeling (TUNEL) assay. The apoptotic cells were increased with the regression of CL, especially during the late-luteal stage. The ERS markers glucose-regulated protein 78 (Grp78), CCAAT/enhancer-binding protein homologous protein (CHOP), X-box binding protein 1 (XBP1), activating transcription factor 6α (ATF6α), eukaryotic initiation factor 2α (eIF2α), inositol-requiring protein 1α (IRE1α), caspase 12, and apoptosis marker caspase 3 were analyzed by real-time polymerase chain reaction (PCR) and immunohistochemistry, in agreement with the results of the TUNEL assay; the expression levels of CHOP, caspase 12, and caspase 3 were increased during the process of CL regression. Luteal cells were isolated and cultured in vitro, and the apoptosis of luteal cells was induced by prostaglandin F2α. The ERS was attenuated by the ERS inhibitor tauroursodeoxycholic acid, and the apoptotic rate was analyzed by flow cytometry. The ERS markers Grp78, CHOP, XBP1s, ATF6α, eIF2α, IRE1α, caspase 12, and apoptotic execute marker caspase 3 were analyzed by real-time PCR and immunofluorescence, and the results suggested that the expression of CHOP, caspase 12, and caspase 3 were increased, and there was increased apoptosis of luteal cells. But the expression of IRE1α/XBP1s and eIF2α was not detected. Taken together, the ERS is involved in the CL regression of rats through the CHOP and caspase 12 pathway.

Indexed as

ApoptosisEndoplasmic Reticulum StressLuteolysisActivating Transcription Factor 6AnimalsCaspase 12Caspase 3Cells, CulturedCorpus LuteumDinoprostDNA-Binding ProteinsEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndoribonucleasesEukaryotic Initiation Factor-2FemaleActivating Transcription Factor 6Atf6 protein, ratCasp12 protein, ratCasp3 protein, ratCaspase 12Caspase 3Ddit3 protein, ratDinoprostDNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPEndoribonucleasesErn1 protein, ratEukaryotic Initiation Factor-2GRP78 protein, ratHeat-Shock ProteinsHspa5 protein, mouseMultienzyme ComplexesProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsTranscription Factor CHOPTranscription FactorsX-Box Binding Protein 1Xbp1 protein, mouseXbp1 protein, ratapoptosiscorpus luteum regressionendoplasmic reticulum stressrats

Identifiers

PMID25332219
PMCPMC4519763
OpenAlexW2010536362

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.