SwePub
Sök i LIBRIS databas

  Extended search

WFRF:(Lindholm Mikko)
 

Search: WFRF:(Lindholm Mikko) > Very low-density li...

  • Stollenwerk, Maria M,1959-Lund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups (author)

Very low-density lipoprotein induces interleukin-1beta expression in macrophages

  • Article/chapterEnglish2005

Publisher, publication year, extent ...

  • Elsevier,2005
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:mau-5265
  • https://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-5265URI
  • https://doi.org/10.1016/j.bbrc.2005.07.123DOI
  • https://lup.lub.lu.se/record/142908URI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Elevated plasma level of very low-density lipoprotein (VLDL) is a risk factor for coronary heart disease. We investigated the effect of VLDL on expression of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) in human peripheral blood monocyte-derived macrophages. IL-1beta mRNA and protein expression was analysed by PCR and ELISA, respectively. Caspase activation was assessed by immunoblotting. Apart from potentiating lipopolysaccharide-induced secretion of IL-1beta, VLDL alone induced secretion of IL-1beta from human monocyte-derived macrophages. This effect was suppressed by an inhibitor of caspase-1, the protease which cleaves pro-IL-1beta. VLDL treatment activated caspase-1, as indicated by increased levels of the caspase-1 p20 subunit. Furthermore, VLDL increased IL-1beta mRNA expression, which was associated with activation of transcription factor AP-1. Inhibition of caspase-1 did not influence IL-1beta mRNA expression. In conclusion, VLDL induces IL-1beta mRNA expression, caspase-1 activation, and IL-1beta release from macrophages, suggesting that VLDL can promote inflammation in atherosclerotic lesions.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Lindholm, MarieLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)medf-mli (author)
  • Ares, IsabellaLund University,Lunds universitet,Experimentell patologi, Malmö,Forskargrupper vid Lunds universitet,Experimental Pathology, Malmö,Lund University Research Groups(Swepub:lu)expp-ipo (author)
  • Larsson, AnnaLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)medf-ala (author)
  • Nilsson, JanLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)medf-jni (author)
  • Ares, MikkoLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)medf-mar (author)
  • Kardiovaskulär forskning - immunitet och aterosklerosForskargrupper vid Lunds universitet (creator_code:org_t)

Related titles

  • In:Biochemical and Biophysical Research Communications - BBRC: Elsevier335:2, s. 603-6080006-291X1090-2104

Internet link

Find in a library

To the university's database

Search outside SwePub

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view