Abstract
Immunoglobulin E (lgE) activates immunity by binding to mast cells and basophils. It is well-known that IgE and its receptor, FcɛR1, play a key role in the development of airway inflammation and remodeling in allergic asthma. Recent studies show that IgE also plays an important role in abdominal aortic aneurysm (AAA) pathogenesis. However, the mechanism by which IgE promotes AAA remains unclear. Here we report that in our mouse model, asthma-induced high level of IgE aggravated AAA, but IgE lost this effect on AAA in FcɛR1-/- mice. Our in vitro study revealed that IgE induced smooth muscle cell senescence via upregulating lincRNA-p21 against p21 without altering expression of p53. By this mechanism, IgE accelerated AAA in ApoE-/- mice, which was blocked by knockdown of lincRNA-p21 in both vitro and vivo. This study suggests that IgE actives the lincRNAp21-p21 pathway to induce SMC senescence, which contributes to the formation of AAA, and lincRNA-p21 is a potential therapeutic target for AAA aggravated by asthma.
Highlights
IntroductionImmunoglobulin E (lgE) activates immunity by binding to mast cells and basophils
Immunoglobulin E activates immunity by binding to mast cells and basophils
Our study suggests that IgE promotes the development of abdomi nal aortic aneurysm (AAA) in a large part by inducing smooth muscle cells (SMCs) senescence via a pathway composed of lincRNAp21-p21
Summary
Immunoglobulin E (lgE) activates immunity by binding to mast cells and basophils It is well-known that IgE and its receptor, FcɛR1, play a key role in the development of airway inflammation and remodeling in allergic asthma. Our in vitro study revealed that IgE induced smooth muscle cell senescence via upregulating lincRNA-p21 against p21 without altering expression of p53. By this mechanism, IgE accelerated AAA in ApoE-/- mice, which was blocked by knockdown of lincRNA-p21 in both vitro and vivo. This study suggests that IgE actives the lincRNAp21-p21 pathway to induce SMC senescence, which contributes to the formation of AAA, and lincRNA p21 is a potential therapeutic target for AAA aggravated by asthma. Antigen (Ag)-specific IgE and FceRI on their membrane, secreting a variety of mediators, which contribute to airway inflammation and remodeling in allergic asthma [8]
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