AI Article Synopsis
- Adipogenesis involves changes in the extracellular matrix that help preadipocytes become more spherical and store lipids as they mature.
- Aortic carboxypeptidase-like protein (ACLP) is present in preadipocytes and decreases during fat cell formation, but its levels can be increased by transforming growth factor beta (TGF beta), which requires specific cellular signaling pathways.
- Despite TGF beta inhibiting adipogenesis when added to differentiation medium, having high levels of ACLP in certain preadipocyte clones doesn’t prevent the process of turning into fat cells.
Article Abstract
Adipogenesis is characterized by early remodeling of the extracellular matrix, allowing preadipocytes to adopt a more spherical shape and optimize lipid accumulation as they mature. Aortic carboxypeptidase-like protein (ACLP), found in collagen-rich tissues including adipose tissue, is expressed in 3T3-L1 and 3T3-F442A preadipocytes, and is downregulated during adipogenesis. We now report that ACLP is found in medium conditioned by 3T3-L1 preadipocytes. Transforming growth factor (TGF) beta, a known modulator of fibrillar matrix protein production, increased ACLP expression by 2.4+/-0.4-fold (mean+/-SE; n=3) in 3T3-L1 preadipocytes, through a mechanism that requires p42/44 MAPK activity. Addition of TGFbeta to differentiation medium, which inhibits adipogenesis, raised ACLP levels in 3T3-L1 cells. However, sustained expression of ACLP in stable clones of 3T3-L1 or 3T3-F442A preadipocytes did not interfere with adipogenesis.
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| http://dx.doi.org/10.1016/j.yexcr.2005.04.031 | DOI Listing |
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