TNF-alpha-induced self expression in human lung endothelial cells is inhibited by native and oxidized alpha 1-antitrypsin

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Subramaniyam, DevipriyaLund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine (author)

TNF-alpha-induced self expression in human lung endothelial cells is inhibited by native and oxidized alpha 1-antitrypsin

Article/chapterEnglish2008

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Elsevier BV,2008

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LIBRIS-ID:oai:lup.lub.lu.se:069bf33f-590e-4c5e-9980-10546fa6b1f3
https://lup.lub.lu.se/record/1200208URI
https://doi.org/10.1016/j.biocel.2007.07.016DOI
https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-16856URI
https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-17561URI

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Language:English
Summary in:English

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Endothelial cells are among the main physiological targets of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). In endothelial cells TNF-alpha elicits a broad spectrum of biological effects including differentiation, proliferation and apoptosis. alpha 1-antitrypsin (AAT), an endogenous inhibitor of serine proteases plays a vital role in protecting host tissue from proteolytic injury at sites of inflammation. Recently, it has been shown that AAT can be internalized by pulmonary endothelial cells, raising speculation that it may modulate endothelial cell function in addition to suppressing protease activity. Using Affymetrix microarray technology, real time PCR and ELISA methods we have investigated the effects of AAT on un-stimulated and TNF-alpha stimulated human primary lung microvascular endothelial cell gene expression and protein secretion. We find that AAT and TNF-alpha generally induced expression of distinct gene families with AAT exhibiting little activity in terms of inflammatory gene expression. Approximately 25% of genes up regulated by TNF-alpha were inhibited by co-administration of AAT including TNF-alpha-induced self expression. Surprisingly, the effects of AAT on TNF-alpha-induced self expression was inhibited equally well by oxidized AAT, a modified form of AAT, which lacks serine protease inhibitor activity. Overall, the pattern of gene expression regulated by native and oxidized AAT was similar with neither inducing pro-inflammatory gene expression. These findings suggest that inhibitory effects of native and oxidized forms of AAT on TNF-alpha stimulated gene expression may play an important role in limiting the uncontrolled endothelial cell activation and vascular injury in inflammatory disease.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Reumatologi och inflammation hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Rheumatology and Autoimmunity hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Neurologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Neurology hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng
SAMHÄLLSVETENSKAP Psykologi hsv//swe
SOCIAL SCIENCES Psychology hsv//eng
alpha 1-Antitrypsin
affymetrix microarray technology
inflammation
oxidized
lung microvascular endothelial cells
Psychology

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Virtala, Robert (author)
Pawlowski, Krzysztof (author)
Clausen, Ib Groth (author)
Warkentin, SiegbertLund University,Lunds universitet,Klinisk minnesforskning,Forskargrupper vid Lunds universitet,Clinical Memory Research,Lund University Research Groups,Lund Univ, Malmo Univ Hosp, Dept Clin Sci, S-22100 Lund, Sweden,University Hospital Malmö, Sweden;Lund University, Sweden(Swepub:lnu)siwaaa (author)
Stevens, Tim (author)
Janciauskiene, SabinaLund University,Lunds universitet,Enheten för kroniska inflammatoriska och degenerativa sjukdomar,Forskargrupper vid Lunds universitet,Chronic Inflammatory and Degenerative Diseases Research Unit,Lund University Research Groups(Swepub:lu)medf-sja (author)
Institutionen för kliniska vetenskaper, MalmöMedicinska fakulteten (creator_code:org_t)

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In:International Journal of Biochemistry & Cell Biology: Elsevier BV40:2, s. 258-2711878-58751357-2725

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MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Clinical Medicin ...; and Rheumatology and ...

MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Clinical Medicin ...; and Neurology

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