Evidence map›Paper›PMID 26899569›Full record

ArticleInflammation2016

Increased TMEM16A Involved in Alveolar Fluid Clearance After Lipopolysaccharide Stimulation.

Honglin Li, Xixin Yan, Rongqin Li, Aili Zhang, Zhiyun Niu, Zhigang Cai, Weisong Duan, Xia Li, Huiran Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    Review
  2. The diverse roles of TMEM16A CaJournal of advanced research · 2021
    Review
  3. Dual role of CaCell death & disease · 2020
    Article
  4. Review
  5. 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 at 3 institutions in 1 country.

Honglin LiDepartment of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China.
Xixin YanDepartment of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China. yanxixin621108@sina.com.
Rongqin LiDepartment of Centralab, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Aili ZhangDepartment of Respirology, Hebei General Hospital, Shijiazhuang, China.
Zhiyun NiuDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Zhigang CaiDepartment of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China.
Weisong DuanDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xia LiDepartment of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China.
Huiran ZhangDepartment of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China.
Second Hospital of Hebei Medical University · CNHebei Medical University · CNHebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledTransmembrane protein 16A (TMEM16A) regulates a wide variety of cellular activities, including epithelial fluid secretion and maintenance of ion homeostasis. Lipopolysaccharide (LPS), an outer membrane component of Gram-negative bacteria, is one of the major causes of acute lung injury (ALI). In this study, we investigated the effects of LPS on the expression of TMEM16A in LA795 cells and mouse lung tissue and the potential mechanism.

resultWe detected the expression of TMEM16A in LA795 cells and mouse lung tissue by RT-PCR, Western blot, and RNA interference techniques. TMEM16A expression was significantly increased by LPS stimulation in LA795 cells and in mouse lung tissue. Moreover, the LPS-induced TMEM16A expression enhancement in lung tissue was much more prominent in the alveolar epithelial region than in bigger airway epithelial cells. The typical TMEM16A current was recorded, and LPS treatment significantly enhances the current amplitude in LA795 cells. TMEM16A shRNA or TMEM16A inhibitor (T16Ainh-A01) did not affect alveolar fluid clearance (AFC), while co-application of T16Ainh-A01 induced a stronger AFC inhibition than LPS alone. LPS notably and synchronously enhanced Akt phosphorylation (p-Akt) and TMEM16A expression in a time-dependent manner in LA795 cells. Taken together, our results suggest that TMEM16A maybe plays an important role in pathological conditions of LPS-induced ALI as a protective protein.

Indexed as

Acute Lung InjuryAnimalsAnoctamin-1Bronchoalveolar Lavage FluidCell Line, TumorChloride ChannelsDisease Models, AnimalLipopolysaccharidesLungMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktPulmonary AlveoliANO1 protein, mouseAnoctamin-1Chloride ChannelsLipopolysaccharidesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPyrimidinesRNA, Small InterferingT16AInh-A01Thiazolesacute lung injuryalveolar fluid clearancelipopolysaccharidep-AktTMEM16A

Identifiers

PMID26899569
OpenAlexW2279412549

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.