Evidence map›Paper›PMID 35027824›Full record

ArticleInternational journal of chronic obstructive pulmonary disease

Effect of Smoking and Its Cessation on the Transcript Profile of Peripheral Monocytes in COPD Patients.

Anjali Trivedi, Geetanjali Bade, Karan Madan, Muzaffer Ahmed Bhat, Randeep Guleria, Anjana Talwar

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Article in International journal of chronic obstructive pulmonary disease. 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
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Anjali TrivediDepartment of Physiology, All India Institute of Medical Sciences, New Delhi, India.
Geetanjali BadeDepartment of Physiology, All India Institute of Medical Sciences, New Delhi, India.
Karan MadanDepartment of Pulmonary, Critical Care and Sleep Medicine, All India Institute of Medical Sciences, New Delhi, India.
Muzaffer Ahmed BhatDepartment of Physiology, All India Institute of Medical Sciences, New Delhi, India.
Randeep GuleriaDepartment of Pulmonary, Critical Care and Sleep Medicine, All India Institute of Medical Sciences, New Delhi, India.
Anjana TalwarDepartment of Physiology, All India Institute of Medical Sciences, New Delhi, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleSmoking is the primary cause of chronic obstructive pulmonary disease (COPD); however, only 10-20% of smokers develop the disease suggesting possible genomic association in the causation of the disease. In the present study, we aimed to explore the whole genome transcriptomics of blood monocytes from COPD smokers (COPD-S), COPD Ex-smokers (COPD-ExS), Control smokers (CS), and Control Never-smokers (CNS) to understand the differential effects of smoking, COPD and that of smoking cessation.

methodsExploratory analyses in form of principal component analysis (PCA) and hierarchical component analysis (uHCA) were performed to evaluate the similarity in gene expression patterns, while differential expression analyses of different supervised groups of smokers and never smokers were performed to study the differential effect of smoking, COPD and smoking cessation. Differentially expressed genes among groups were subjected to post-hoc enrichment analysis. Candidate genes were subjected to external validation by quantitative RT-PCR experiments.

resultsCNS made a cluster completely segregated from the other three subgroups (CS, COPDS and COPD-ExS). About 550, 8 and 5 genes showed differential expression, respectively, between CNS and CS, between CS and COPD-S, and between COPD-S and COPD-ExS. Apoptosis, immune response, cell adhesion, and inflammation were the top process networks identified in enrichment analysis. Two candidate genes (CASP9 and TNFRSF1A) found to be integral to several pathways in enrichment analysis were validated in an external validation experiment.

conclusionControl never smokers had formed a cluster distinctively separated from all smokers (COPDS, COPD-ExS, and CS), while amongst all smokers, control smokers had aggregated in a separate cluster. Smoking cessation appeared beneficial if started at an early stage as many genes altered due to smoking started reverting towards the baseline, whereas only a few COPD-related genes showed reversal after smoking cessation.

Indexed as

Pulmonary Disease, Chronic ObstructiveSmoking CessationHumansMonocytesSmokersSmokingapoptosiscell adhesionchronic obstructive pulmonary diseaseimmune responsesmoking

Identifiers

PMID35027824
PMCPMC8749770

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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.