The Role of the Buccal Fat Pad in Facial Aesthetic Surgery

Social media have triggered a buccal fat pad excision frenzy. Not surprisingly, there is tremendous appeal of having a slimmer lower face and more defined jawline after undergoing a small intraoral procedure under local anesthesia. Although this procedure is great for social media and seemingly beneficial for jawline aesthetics, the evidence remains limited as to whether or not this is an effective long-term solution. How much the buccal fat pad persists or diminishes as we age is an area of debate. However, the possibility of causing premature aging and midface distortion in the long run is disconcerting

Data from: Th2 cytokines inhibit lymphangiogenesis

Lymphangiogenesis is the process by which new lymphatic vessels grow in response to pathologic stimuli such as wound healing, inflammation, and tumor metastasis. It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis

Th2 cytokines inhibit lymphangiogenesis.

Lymphangiogenesis is the process by which new lymphatic vessels grow in response to pathologic stimuli such as wound healing, inflammation, and tumor metastasis. It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis

Inhibition of Inflammation and iNOS Improves Lymphatic Function in Obesity

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rhIL-4 and rhIL-13 inhibit hLEC tubule formation.

<p><b>A.</b> Representative images of cultured hLECs tubule formation on matrigel after treatment with 50 ng/ml rhIL-4 or rhIL-13 protein, or media alone (control) for 12 hours. <b>B.</b> Quantification of tubule formation per high-power field. Control vs. rhIL-4 (n = 5–8 in each; *p<0.01); control vs. rhIL-13 (n = 5–8 in each; *p<0.01); rhIL-4 vs. rhIL-13 (n = 5–8 in each; p = NS).</p

rhIL-4 and rhIL-13 inhibit hLEC migration.

<p><b>A.</b> Representative images of cultured hLECs after scratch wound and treatment with 50 ng/ml rhIL-4 or rhIL-13 protein, or media alone (control) at 0, 12 and 24 hours. White dotted lines represent LEC migration borders. Black solid lines represent initial gap created by scratch. <b>B.</b> Quantification of hLEC migration at 12 and 24 hours. Control vs. rhIL-4 (n = 5 in each; *p<0.01 for both time points); control vs. rhIL-13 (n = 5 in each; *p<0.01 for both time points); rhIL-4 vs. rhIL-13 (n = 5 in each; p = NS for both time points).</p

IL-4 and IL-13 blockade does not increase corneal angiogenesis.

<p><b>A.</b> Representative immunofluorescent cornea whole mount images stained for CD31 and LYVE-1. Scale bar = 100μm. <b>B.</b> Quantification of blood vessel area per 0.25mm². Control vs. IL-4mAb (n = 8 in each; p = NS); control vs. IL-13mAb (n = 8 in each; p = NS); IL-4mAb vs. IL-13mAb (n = 8 in each; p = NS). <b>C.</b> Quantification of blood vessel volume per 0.25mm². Control vs. IL-4mAb (n = 8 in each; p = NS); control vs. IL-13mAb (n = 8 in each; p = NS); IL-4mAb vs. IL-13mAb (n = 8 in each; p = NS).</p