Evidence map›Paper›PMID 31127489›Full record

ArticleHuman cell2019

Inhibition of angiotensin II-induced cerebrovascular smooth muscle cell proliferation by LRRC8A downregulation through suppressing PI3K/AKT activation.

Jingjing Lu, Feng Xu, Jiewen Zhang

Abstract read
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In one paragraph

Article in Human cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Upregulation of LRRC8A by mInternational journal of biological sciences · 2023
    Article
  10. Article
  11. LRRC8A influences the growth of gastric cancer cells via the p53 signaling pathway.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
    Article
  12. Article
  13. Article
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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

3 authors at 2 institutions in 1 country.

Jingjing LuDepartment of Neurology, People's Hospital of Zhengzhou University, No. 7 Wai-5 Road, Zhengzhou, 450052, Henan, China.
Feng XuDepartment of Urology, First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Jiewen ZhangDepartment of Neurology, People's Hospital of Zhengzhou University, No. 7 Wai-5 Road, Zhengzhou, 450052, Henan, China. HZ_Sammy@163.com.
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebrovascular smooth muscle cell proliferation is the major contributor to cerebrovascular remodeling and stroke. Chloride channels have been suggested to play an important role in the regulation of smooth muscle cell proliferation. This study aims to investigate the effect of leucine-rich repeat-containing 8A (LRRC8A), an essential component of volume-sensitive chloride channels, on cerebrovascular smooth muscle cell proliferation. The data showed that LRRC8A expression was increased in mouse brain artery during angiotensin II (AngII)-induced cerebrovascular remodeling. Similarly, AngII also increased the expression of LRRC8A in human brain vascular smooth muscle cells (HBVSMCs). Knockdown of LRRC8A by siRNA significantly inhibited AngII-induced the proliferation, migration, and invasion in HBVSMCs. The inhibition of HBVSMCs proliferation by LRRC8A downregulation appeared to be involved in suppression of cell-cycle transition. AngII-induced the decrease in p21 and p27 expression and the increase in CDK4 and cyclin D1 expression were attenuated by LRRC8A downregulation. Moreover, inhibition of LRRC8A suppressed AngII-induced PI3K/AKT activation and reactive oxygen species generation, but had no effect on JNK, ERK, and p38 phosphorylation. In addition, activation of PI3K/AKT-signaling pathways with specific agonists significantly abolished the effect of LRRC8A deficiency on HBVSMC proliferation. This present study demonstrates that knockdown of LRRC8A ameliorates AngII-induced cerebrovascular smooth muscle cell proliferation via inhibiting PI3K/AKT pathway, suggesting that LRRC8A may be a novel molecular target in the treatment of vascular remodeling and stroke.

Indexed as

Down-RegulationAngiotensin IIAnimalsCell CycleCell ProliferationCells, CulturedGene ExpressionHumansMaleMembrane ProteinsMice, Inbred C57BLMolecular Targeted TherapyMuscle, Smooth, VascularPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAngiotensin IILRRC8A protein, humanMembrane ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesRNA, Small InterferingAngiotensin IICell cycleCerebrovascular smooth muscle cellsLRRC8API3K/AKT signalingProliferation

Identifiers

PMID31127489
OpenAlexW2946376759

What OpenQuestion holds

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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.