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No functional role of plasminogen activator inhibitor‐1 in murine adipogenesis or adipocyte differentiation
Author(s) -
SCROYEN I.,
CHRISTIAENS V.,
LIJNEN H. R.
Publication year - 2007
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2006.02284.x
Subject(s) - adipogenesis , matrigel , adipocyte , adipose tissue , in vivo , chemistry , plasminogen activator , in vitro , microbiology and biotechnology , 3t3 l1 , endocrinology , medicine , embryonic stem cell , plasminogen activator inhibitor 1 , biology , biochemistry , gene
Summary. Objective: To substantiate a potential role of plasminogen activator inhibitor‐1 (PAI‐1) in adipogenesis, we have studied its effects on in vitro adipocyte differentiation and on in vivo adipose tissue formation. Results: Our in vitro data do not support a functional role of PAI‐1, as substantiated by our findings that: (i) inhibition of PAI‐1 with a neutralizing antibody did not affect differentiation of 3T3‐F442A preadipocytes; (ii) overexpression of murine PAI‐1 in 3T3‐F442A cells had no effect on differentiation; and (iii) differentiation of PAI‐1‐deficient murine embryonic fibroblasts into mature adipocytes was comparable to wild‐type (WT) cells. Furthermore, our in vivo studies did not reveal an important role for PAI‐1, as suggested by our findings that: (i) de novo fat pad formation in NUDE mice following injection of 3T3‐F442A cells was not affected by a PAI‐1 neutralizing antibody; and (ii) adipose tissue formation following combined injection of Matrigel and basic fibroblast growth factor was comparable in WT and in PAI‐1 deficient mice. Conclusion: Taken together, these in vitro and in vivo studies in murine model systems do not support an important functional role of PAI‐1 in adipogenesis.