PMID- 8840272
OWN - NLM
STAT- MEDLINE
DCOM- 19961227
LR  - 20220227
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 50
IP  - 2
DP  - 1996 Aug
TI  - Mesangial cell-derived transforming growth factor-beta 1 reduces macrophage 
      adhesiveness with consequent deactivation.
PG  - 445-52
AB  - Adhesion of macrophages is a crucial event that determines the number and 
      function of macrophages at inflammatory sites. The aim of this study was to 
      elucidate the role of mesangial cells in the regulation of macrophage 
      adhesiveness. J774.2 macrophages were suspended in serial dilutions of mesangial 
      cell conditioned medium (MC medium) and seeded on plastic tissue culture plates. 
      MC medium did not affect the initial adhesion of macrophages but induced 
      subsequent detachment in a concentration-dependent manner. A similar effect was 
      observed when macrophages were plated on plastic coated with laminin, collagen 
      type IV or Matrigel. The reduced adhesiveness was reversible, and cell viability 
      was unaffected by MC medium, indicating that the effect is not due to 
      cytotoxicity. Conditioned media from fibroblastic, epithelial and endothelial 
      cell lines did not induce macrophage detachment. To identify the active component 
      in MC medium, we examined the involvement of transforming growth factor-beta 1 
      (TGF-beta 1) in the process. Mesangial cells constitutively expressed TGF-beta 1 
      mRNA, and MC medium contained the active form of TGF-beta 1. Exogenously added 
      TGF-beta 1 induced macrophage detachment in a dose-dependent manner, and an 
      anti-TGF-beta 1 neutralizing antibody partially abolished the activity of MC 
      medium, indicating the involvement of TGF-beta 1 as an active component. Compared 
      to adherent cells, detached macrophages showed reduced mitogenic activity and 
      blunted induction of IL-1 beta and IL-6 in response to lipopolysaccharide. These 
      data demonstrate that TGF-beta 1 is a mesangial cell-derived factor that impairs 
      adhesiveness of macrophages and confers blunted responses to a specific stimulus. 
      These findings suggest one potential mechanism for macrophage clearance from 
      inflamed glomeruli.
FAU - Suto, T S
AU  - Suto TS
AD  - Department of Medicine, University College London Medical School, England, United 
      Kingdom.
FAU - Fine, L G
AU  - Fine LG
FAU - Kitamura, M
AU  - Kitamura M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Cell Adhesion/drug effects/*physiology
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Culture Media, Conditioned
MH  - Gene Expression
MH  - Glomerular Mesangium/cytology/*physiology
MH  - Interleukin-1/biosynthesis/genetics
MH  - Interleukin-6/biosynthesis/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages/cytology/drug effects/*physiology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Transforming Growth Factor beta/pharmacology/*physiology
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - S0085-2538(15)59629-4 [pii]
AID - 10.1038/ki.1996.335 [doi]
PST - ppublish
SO  - Kidney Int. 1996 Aug;50(2):445-52. doi: 10.1038/ki.1996.335.