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Obesity in Angiogenesis and Regenerative Lung Growth after Pneumonectomy
Author(s) -
Mammoto Tadanori,
Hunyenyiwa Tendai,
Hendee Kathryn,
Matus Kienna,
Mammoto Akiko
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.01940
Subject(s) - angiogenesis , vascular endothelial growth factor , leptin , endocrinology , regeneration (biology) , medicine , lung , biology , population , microbiology and biotechnology , obesity , vegf receptors , environmental health
Obese population is rapidly growing worldwide. Obesity is associated with impairment of wound healing and tissue regeneration. Angiogenesis, the formation of new blood capillaries, plays a key role in organ regeneration and repair. We and other groups have reported that inhibition of angiogenesis attenuates lung growth after unilateral pneumonectomy (PNX) and that obesity is accompanied by endothelial cell dysfunction. However, the effects of obesity on lung regeneration remain unclear. Compensatory lung growth and vascular and alveolar morphogenesis after PNX are suppressed in leptin‐deficient ob/ob mice treated with high‐fat diet compared to that in control lean mice. The levels of the major angiogenic factor, vascular endothelial growth factor (VEGF) are higher in the serum and the lung tissue collected from post‐PNX mice compared to those from sham‐operated control mice, while these effects are attenuated in post‐PNX leptin‐deficient ob/ob mice with high‐fat diet. Among various VEGF isoforms, VEGF164, but not VEGF188 and VEGF120, increases in the post‐PNX mouse lungs, while these effects are inhibited in obese mice. These results suggestthat obesity inhibits post‐PNX regenerative lung growth through VEGF164 signaling. Modulation of VEGF signaling may be the efficient strategy to restore lung regeneration and repair in obese people.