Linked Life Data

18655827

Source:http://linkedlifedata.com/resource/pubmed/id/18655827

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-8-25
pubmed:abstractText
Phenotypic expression of alpha-smooth muscle actin (alpha-SMA), a smooth muscle marker, has been implicated in vascular diseases, fibrosis, wound healing, and tissue remodeling. Bradykinin (BK), a vasoactive peptide produced during tissue injury, plays a key role in inflammatory and vascular responses associated with tissue injury. In the present study, we demonstrated for the first time that BK treatment increased alpha-SMA expression in human adipose tissue-derived mesenchymal stem cells (hADSCs). This BK-induced alpha-SMA expression was abrogated by small interfering RNA (siRNA)-mediated depletion of endogenous myocardin, a transcription factor involved in smooth muscle differentiation. BK also increased the intracellular calcium concentration ([Ca(2+)](i)), a response that was completely blocked by treatment with a BK B2 receptor-specific antagonist (HOE 140), suggesting that the BK B2 receptor was participating in BK-induced cellular responses. In addition, BK induced the secretion of transforming growth factor-beta1 (TGF-beta1) and autocrine activation of Smad2. Pretreatment with a TGF-beta type I receptor kinase inhibitor (SB-431542), small interfering RNA-mediated depletion of endogenous Smad2, or adenoviral expression of Smad7 (an inhibitory Smad isoform) all blocked BK-induced alpha-SMA expression and Smad2 phosphorylation. Furthermore, a MEK-specific inhibitor (U0126) abrogated BK-induced TGF-beta1 secretion, Smad2 phosphorylation, and alpha-SMA expression. These results suggest that BK induced expression of alpha-SMA in hADSCs through ERK-dependent activation of the autocrine TGF-beta1-Smad2 crosstalk pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1882-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18655827-Actins, pubmed-meshheading:18655827-Adipose Tissue, pubmed-meshheading:18655827-Autocrine Communication, pubmed-meshheading:18655827-Bradykinin, pubmed-meshheading:18655827-Calcium, pubmed-meshheading:18655827-Cells, Cultured, pubmed-meshheading:18655827-Dose-Response Relationship, Drug, pubmed-meshheading:18655827-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:18655827-Humans, pubmed-meshheading:18655827-Intracellular Space, pubmed-meshheading:18655827-Mesenchymal Stem Cells, pubmed-meshheading:18655827-Muscle, Smooth, pubmed-meshheading:18655827-Nuclear Proteins, pubmed-meshheading:18655827-Phosphorylation, pubmed-meshheading:18655827-Receptor, Bradykinin B2, pubmed-meshheading:18655827-Smad2 Protein, pubmed-meshheading:18655827-Stress Fibers, pubmed-meshheading:18655827-Time Factors, pubmed-meshheading:18655827-Trans-Activators, pubmed-meshheading:18655827-Transforming Growth Factor beta1
pubmed:year
2008
pubmed:articleTitle
Bradykinin-induced expression of alpha-smooth muscle actin in human mesenchymal stem cells.
pubmed:affiliation
Department of Physiology, School of Medicine, Pusan National University, Busan 602-739, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't