Key result
Angiopoietin-1 protected 3T3-L1 preadipocytes from saturated fatty acid-induced apoptosis and endoplasmic reticulum stress by increasing Bcl-x and decreasing Casp-8 expression.
Why the study?
Little is known about mechanisms controlling cross talk between endothelial cells and adipocytes, or how angiogenesis is involved in adipocyte physiology.
Angiopoietin-1 protects preadipocytes from saturated fatty acid-induced apoptosis and endoplasmic reticulum stress, highlighting a potential role for angiogenesis factors in adipocyte physiology.
Cross talk between endothelial cells and adipocytes is vital to adipocyte functions, but little is known about the mechanisms or factors controlling the process. Angiogenesis is a critical component linking the endothelium to healthy adipogenesis, yet it is not known if or how it is involved in adipocyte physiology. Therefore, the purpose of this study was to determine the effect of angiopoietin-1 (Ang-1) and -2 (Ang-2) as well as their receptor, Tie-2, on adipocyte physiology. 3T3-L1 pre- and mature adipocytes were found to express Ang-1, Ang-2, and Tie-2, which decrease upon polyunsaturated fatty acid treatment. Furthermore, 3T3-L1 cells treated with recombinant Ang-1 or Ang-2 increased expression of the antiapoptotic gene Bcl-x and decreased expression of the proapoptotic gene Casp-8. Next, preadipocytes were treated with saturated fatty acids (SFAs) to induce cell stress. SFA-mediated splicing of X-box-binding protein-1 was reduced by co-treatment with Ang-1, and cell viability was improved in the presence of SFAs + Ang-1. Taken together, these results indicate that Ang-1 may protect preadipocytes from SFA-induced apoptosis and endoplasmic reticulum stress.
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Son et al. (2020) studied Adipocyte physiology and cell stress. Angiopoietin-1 (Ang-1) and Angiopoietin-2 (Ang-2) vs. Untreated or saturated fatty acids alone was evaluated on Cell viability, apoptosis, and endoplasmic reticulum stress. Angiopoietin-1 protected 3T3-L1 preadipocytes from saturated fatty acid-induced apoptosis and endoplasmic reticulum stress by increasing Bcl-x and decreasing Casp-8 expression.
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