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Sökning: WFRF:(Larsson Callerfelt Anna Karin) > Altered hypoxia-ind...

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FältnamnIndikatorerMetadata
00005837naa a2200457 4500
001oai:lup.lub.lu.se:a540550d-2930-451b-acae-902827c962e7
003SwePub
008240826s2024 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/a540550d-2930-451b-acae-902827c962e72 URI
0247 a https://doi.org/10.1186/s12931-024-02907-x2 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Ryde, Martinu Lund University,Lunds universitet,Lungbiologi,Forskargrupper vid Lunds universitet,Lungmedicin, allergologi och palliativ medicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Lungfysiologi och biomarkörer,Lung Biology,Lund University Research Groups,Respiratory Medicine, Allergology, and Palliative Medicine,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lung physiology and biomarkers4 aut0 (Swepub:lu)ma8727ry
2451 0a Altered hypoxia-induced cellular responses and inflammatory profile in lung fibroblasts from COPD patients compared to control subjects
264 1c 2024
520 a Background: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by chronic bronchitis, emphysema and vascular remodelling. The disease is associated with hypoxia, inflammation and oxidative stress. Lung fibroblasts are important cells in remodelling processes in COPD, as main producers of extracellular matrix proteins but also in synthesis of growth factors and inflammatory mediators. Methods: In this study we aimed to investigate if there are differences in how primary distal lung fibroblasts obtained from COPD patients and healthy subjects respond to hypoxia (1% O2) and pro-fibrotic stimuli with TGF-β1 (10 ng/mL). Genes and proteins associated with oxidative stress, endoplasmic reticulum stress, remodelling and inflammation were analysed with RT-qPCR and ELISA. Results: Hypoxia induced differences in expression of genes involved in oxidative stress (SOD3 and HIF-1α), ER stress (IRE1, PARK and ATF6), apoptosis (c-Jun and Bcl2) and remodelling (5HTR2B, Collagen7 and VEGFR2) in lung fibroblasts from COPD subjects compared to control subjects, where COPD fibroblasts were in general less responsive. The release of VEGF-C was increased after hypoxia, whereas TGF-β significantly reduced the VEGF response to hypoxia and the release of HGF. COPD fibroblasts had a higher release of IL-6, IL-8, MCP-1 and PGE2 compared to lung fibroblasts from control subjects. The release of inflammatory mediators was less affected by hypoxia, whereas TGFβ1 induced differences in inflammatory profile between fibroblasts from COPD and control subjects. Conclusion: These results suggest that there is an alteration of gene regulation of various stress responses and remodelling associated mediator release that is related to COPD and hypoxia, where fibroblasts from COPD patients have a deficient response.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Lungmedicin och allergi0 (SwePub)302192 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Respiratory Medicine and Allergy0 (SwePub)302192 hsv//eng
653 a COPD
653 a ER stress
653 a Gene expression
653 a Hypoxia
653 a Inflammation
653 a Lung fibroblasts
653 a Oxidative stress
653 a Remodelling
7001 a Marek, Norau Lund University4 aut
7001 a Löfdahl, Annau Lund University,Lunds universitet,Lungbiologi,Forskargrupper vid Lunds universitet,Lung Biology,Lund University Research Groups4 aut0 (Swepub:lu)med-amh
7001 a Pekny, Oliviau Lund University4 aut
7001 a Bjermer, Leifu Lund University,Lunds universitet,Lungmedicin, allergologi och palliativ medicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Klinisk lungmedicin,Forskargrupper vid Lunds universitet,Respiratory Medicine, Allergology, and Palliative Medicine,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Clinical Respiratory Medicine,Lund University Research Groups4 aut0 (Swepub:lu)lung-lbj
7001 a Westergren-Thorsson, Gunillau Lund University,Lunds universitet,Lungbiologi,Forskargrupper vid Lunds universitet,Lund University Bioimaging Center,Medicinska fakulteten,WCMM- Wallenberg center för molekylär medicinsk forskning,Lung Biology,Lund University Research Groups,Faculty of Medicine,WCMM-Wallenberg Centre for Molecular Medicine4 aut0 (Swepub:lu)medk-gwt
7001 a Tufvesson, Ellenu Lund University,Lunds universitet,Lungmedicin, allergologi och palliativ medicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Neonatologi,Forskargrupper vid Lunds universitet,Tornbladinstitutet,Lungfysiologi och biomarkörer,Respiratory Medicine, Allergology, and Palliative Medicine,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Neonatology,Lund University Research Groups,Tornblad Institute,Lung physiology and biomarkers4 aut0 (Swepub:lu)medk-etu
7001 a Larsson Callerfelt, Anna-Karinu Lund University,Lunds universitet,Lungbiologi,Forskargrupper vid Lunds universitet,LTH profilområde: Aerosoler,LTH profilområden,Lunds Tekniska Högskola,Lung Biology,Lund University Research Groups,LTH Profile Area: Aerosols,LTH Profile areas,Faculty of Engineering, LTH4 aut0 (Swepub:lu)med-ail
7102 a Lungbiologib Forskargrupper vid Lunds universitet4 org
7730 t Respiratory Researchg 25:1q 25:1x 1465-9921
8564 u http://dx.doi.org/10.1186/s12931-024-02907-xx freey FULLTEXT
8564 8u https://lup.lub.lu.se/record/a540550d-2930-451b-acae-902827c962e7
8564 8u https://doi.org/10.1186/s12931-024-02907-x

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