Evidence map›Paper›PMID 39578839›Full record

ArticleCell communication and signaling : CCS2024

Mitochondrial dysfunction and impaired DNA damage repair through PICT1 dysregulation in alveolar type II cells in emphysema.

Hannah Simborio, Hassan Hayek, Beata Kosmider, John W Elrod, Sudhir Bolla, Nathaniel Marchetti, Gerard J Criner, Karim Bahmed

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2024. 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
–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

5 citing papers in PubMed.

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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

8 authors.

Hannah SimborioCenter for Inflammation and Lung Research, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Hassan HayekCenter for Inflammation and Lung Research, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Beata KosmiderCenter for Inflammation and Lung Research, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
John W ElrodAging & Cardiovascular Discovery Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA.
Sudhir BollaDepartment of Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA.
Nathaniel MarchettiDepartment of Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA.
Gerard J CrinerDepartment of Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA.
Karim BahmedCenter for Inflammation and Lung Research, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA, 19140, USA. karim.bahmed@temple.edu.

Funding

Regulation of alveolar epithelial regeneration by T cellsR01HL150587 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOSMIDER, BEATA, TIAN, YING · 2020 to 2023
$2.2M
Alveolar Epithelial Cell Dysfunction Induced By Flavored E-Cigarette AerosolsR01ES032081 · NIEHS · TEMPLE UNIV OF THE COMMONWEALTH · PI KOSMIDER, BEATA · 2020 to 2024
$1.9M
Cigarette smoke influences alveolar type II cell-derived exosomesR21ES030808 · NIEHS · TEMPLE UNIV OF THE COMMONWEALTH · PI BAHMED, KARIM · 2020 to 2021
$434k
NHLBI NIH HHS R01 HL150587NIEHS NIH HHS R01 ES032081NIEHS NIH HHS R21 ES030808NIH HHS ES030808NIH HHS ES032081U.S. Department of Defense DoD W81XWH2110414U.S. Department of Defense W81XWH2110400
6 · The paper itself

Abstract

backgroundAlveolar type II (ATII) cells have a stem cell potential in the adult lung and repair the epithelium after injury induced by harmful factors. Their damage contributes to emphysema development, characterized by alveolar wall destruction. Cigarette smoke is the main risk factor for this disease development.

methodsATII cells were obtained from control non-smoker and smoker organ donors and emphysema patients. Isolated cells were used to study the role of PICT1 in this disease. Also, a cigarette smoke-induced murine model of emphysema was applied to define its function in disease progression further.

resultsDecreased PICT1 expression was observed in human and murine ATII cells in emphysema. PICT1 was immunoprecipitated, followed by mass spectrometry analysis. We identified MRE11, which is involved in DNA damage repair, as its novel interactor. PICT1 and MRE11 protein levels were decreased in ATII cells in this disease. Moreover, cells with PICT1 deletion were exposed to cigarette smoke extract. This treatment induced cellular and mitochondrial ROS, cell cycle arrest, nuclear and mitochondrial DNA damage, decreased mitochondrial respiration, and impaired DNA damage repair.

conclusionsThis study indicates that PICT1 dysfunction can negatively affect genome stability and mitochondrial activity in ATII cells, contributing to emphysema development. Targeting PICT1 can lead to novel therapeutic approaches for this disease.

Indexed as

DNA DamageDNA RepairMitochondriaAlveolar Epithelial CellsAnimalsHumansMaleMiceMice, Inbred C57BLMRE11 Homologue ProteinPulmonary EmphysemaReactive Oxygen SpeciesTumor Suppressor ProteinsMRE11 Homologue ProteinMRE11 protein, humanReactive Oxygen SpeciesTumor Suppressor ProteinsApoptosisATII cellsCell cycleCOPDDouble strand breaksMitochondrial respirationOxidative stressOXPHOS

Identifiers

PMID39578839
PMCPMC11583753

What Socratic holds

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LicenceCC BY
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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 Socratic graph.