| Autor: |
Yair Romero, Yalbi Itzel Balderas-Martínez, Miguel Angel Vargas-Morales, Manuel Castillejos-López, Joel Armando Vázquez-Pérez, Jazmín Calyeca, Luz María Torres-Espíndola, Nelly Patiño, Angel Camarena, Ángeles Carlos-Reyes, Edgar Flores-Soto, Guadalupe León-Reyes, Martha Patricia Sierra-Vargas, Iliana Herrera, Erika Rubí Luis-García, Víctor Ruiz, Rafael Velázquez-Cruz, Arnoldo Aquino-Gálvez |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
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| Zdroj: |
Cells; Volume 11; Issue 19; Pages: 3014 |
| ISSN: |
2073-4409 |
| DOI: |
10.3390/cells11193014 |
| Popis: |
Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by exacerbated extracellular matrix deposition that disrupts oxygen exchange. Hypoxia and its transcription factors (HIF-1α and 2α) influence numerous circuits that could perpetuate fibrosis by increasing myofibroblasts differentiation and by promoting extracellular matrix accumulation. Therefore, this work aimed to elucidate the signature of hypoxia in the transcriptomic circuitry of IPF-derived fibroblasts. To determine this transcriptomic signature, a gene expression analysis with six lines of lung fibroblasts under normoxia or hypoxia was performed: three cell lines were derived from patients with IPF, and three were from healthy donors, a total of 36 replicates. We used the Clariom D platform, which allows us to evaluate a huge number of transcripts, to analyze the response to hypoxia in both controls and IPF. The control′s response is greater by the number of genes and complexity. In the search for specific genes responsible for the IPF fibroblast phenotype, nineteen dysregulated genes were found in lung fibroblasts from IPF patients in hypoxia (nine upregulated and ten downregulated). In this sense, the signaling pathways revealed to be affected in the pulmonary fibroblasts of patients with IPF may represent an adaptation to chronic hypoxia. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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