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IPA Software Analysis Reveals Inflammation and Apoptosis as Major Enrichment Functional Process in Normal Lung During Aging
Author(s) -
Calyeca Jazmin,
Balderas-Martinez Yalbi,
Mora Ana,
Selman Moises,
Pardo Annie
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03548
Subject(s) - transcriptome , biology , inflammation , senescence , proteostasis , microarray analysis techniques , microarray , fibrosis , trem2 , cancer research , bioinformatics , immunology , medicine , microbiology and biotechnology , pathology , gene , gene expression , microglia , genetics
Aging is an irreversible biological process characterized by progressive functional decline and represent an independent risk factor for many chronic‐degenerative diseases. Several hallmarks have been associated to aging including genome instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient‐sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered cellular communication. In lungs, accelerated aging has been associated to some diseases such as idiopathic pulmonary fibrosis and chronic obstructive lung disease. However, the consequences of physiological aging on the lungs remain uncertain. In this study, we aimed to identify the dysregulated genes and pathways occurring in mice lung transcriptome during aging. For this purpose, lungs from 3 young (1‐month‐old) and 3 old (18‐month‐old) C57BL/6 mice were examined. We used Ingenuity Pathway Software analysis on a previous reported transcriptome evaluation performed in our Lab by Microarray technology (GeneChip™ Mouse Gene 2.0 ST Array of Affymetrix). In old lungs, 576 genes were differentially expressed compared with their young counterparts. In the top 10 upregulated pathways revealed by IPA analysis, the highest over‐expressed pathway in old WT lungs was the Triggering receptor expressed on myeloid cells‐1 (TREM‐1) followed by Toll‐like receptor (TLR) signaling and p38 MAPK. According to these findings, the expression of the upstream regulators INFγ, TNF, TLR2, and TLR4 were increased in the lungs of old mice. In addition, among the top five functions from the “diseases and disorders category” we found Respiratory Disease and Inflammatory Response as one of the higher enriched pathways. Finally, extended analysis of the top five functions from the “molecular and cellular functions category” reveals Cell Death and Survival, including Apoptosis of several lung cell populations, as one of the most enriched pathways. Support or Funding Information Supported by CONACYT 281074