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

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Fältnamn	Indikatorer	Metadata
000		05185naa a2200565 4500
001		oai:lup.lub.lu.se:069bf33f-590e-4c5e-9980-10546fa6b1f3
003		SwePub
008		160401s2008 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:DiVA.org:lnu-16856
009		oai:DiVA.org:lnu-17561
024	7	a https://lup.lub.lu.se/record/12002082 URI
024	7	a https://doi.org/10.1016/j.biocel.2007.07.0162 DOI
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-168562 URI
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-175612 URI
040		a (SwePub)lud (SwePub)lnud (SwePub)lnu
041		a engb eng
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a Subramaniyam, Devipriyau Lund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine4 aut0 (Swepub:lu)medf-dsu
245	1 0	a TNF-alpha-induced self expression in human lung endothelial cells is inhibited by native and oxidized alpha 1-antitrypsin
264	1	b Elsevier BV,c 2008
520		a 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.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
650	7	a SAMHÄLLSVETENSKAPx Psykologi0 (SwePub)5012 hsv//swe
650	7	a SOCIAL SCIENCESx Psychology0 (SwePub)5012 hsv//eng
653		a alpha 1-Antitrypsin
653		a affymetrix microarray technology
653		a inflammation
653		a oxidized
653		a lung microvascular endothelial cells
653		a Psychology
700	1	a Virtala, Robert4 aut
700	1	a Pawlowski, Krzysztof4 aut
700	1	a Clausen, Ib Groth4 aut
700	1	a Warkentin, Siegbertu Lund 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, Sweden4 aut0 (Swepub:lnu)siwaaa
700	1	a Stevens, Tim4 aut
700	1	a Janciauskiene, Sabinau Lund University,Lunds universitet,Enheten för kroniska inflammatoriska och degenerativa sjukdomar,Forskargrupper vid Lunds universitet,Chronic Inflammatory and Degenerative Diseases Research Unit,Lund University Research Groups4 aut0 (Swepub:lu)medf-sja
710	2	a Institutionen för kliniska vetenskaper, Malmöb Medicinska fakulteten4 org
773	0	t International Journal of Biochemistry & Cell Biologyd : Elsevier BVg 40:2, s. 258-271q 40:2<258-271x 1878-5875x 1357-2725
856	4	u http://dx.doi.org/10.1016/j.biocel.2007.07.016y FULLTEXT
856	4 8	u https://lup.lub.lu.se/record/1200208
856	4 8	u https://doi.org/10.1016/j.biocel.2007.07.016
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-16856
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-17561

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MEDICIN OCH HÄLSOVETENSKAP: MEDICIN OCH HÄLS ...; och Klinisk medicin; och Reumatologi och ...

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